CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown

Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx">GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Scientific Papers found: Click to Expand⟱
147- AG,  EGCG,  CUR,    Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, MCF-7
Bax:Bcl2↑,
NF-kB↓,
PI3K/Akt↓,
STAT3↓,

3446- ALA,  CUR,    The Potential Protective Effect of Curcumin and α-Lipoic Acid on N-(4-Hydroxyphenyl) Acetamide-induced Hepatotoxicity Through Downregulation of α-SMA and Collagen III Expression
- in-vivo, Nor, NA
*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments

2635- Api,  CUR,    Synergistic Effect of Apigenin and Curcumin on Apoptosis, Paraptosis and Autophagy-related Cell Death in HeLa Cells
- in-vitro, Cerv, HeLa
TumCD↑, Treatment with a combination of apigenin and curcumin increased the expression levels of genes related to cell death in HeLa cells 1.29- to 27.6-fold.
eff↑, combination of curcumin and apigenin showed a synergistic anti-tumor effect
TumAuto↑, autophagic cell death, as well as ER stress-associated paraptosis
ER Stress↑,
Paraptosis↑,
GRP78/BiP↓, GRP78 expression was down-regulated, and massive cytoplasmic vacuolization was observed in HeLa cells
Dose↝, combined use of 0.09 μg/μl curcumin and 0.06 μg/μl apigenin showed a synergistic anti-tumor effect

1024- Api,  CUR,    Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects
- vitro+vivo, Melanoma, A375 - in-vitro, Melanoma, A2058 - in-vitro, Melanoma, RPMI-7951
TumCG↓,
Apoptosis↑,
PD-L1↓, IFN-γ-induced PD-L1 upregulation was significantly inhibited by flavonoids, especially apigenin
STAT1↓,
tumCV↓,
T-Cell↑, Curcumin and apigenin enhance T cell-mediated melanoma cell killing

2703- BBR,  CUR,  SFN,  UA,  GamB  Naturally occurring anti-cancer agents targeting EZH2
- Review, Var, NA
EZH2↓, In fact, several natural products such as curcumin, triptolide, ursolic acid, sulforaphane, davidiin, tanshindiols, gambogic acid, berberine and Alcea rosea have been shown to serve as EZH2 modulators.

3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

1426- Bos,  CUR,  Chemo,    Novel evidence for curcumin and boswellic acid induced chemoprevention through regulation of miR-34a and miR-27a in colorectal cancer
- in-vivo, CRC, NA - in-vitro, CRC, HCT116 - in-vitro, CRC, RKO - in-vitro, CRC, SW480 - in-vitro, RCC, SW-620 - in-vitro, RCC, HT-29 - in-vitro, CRC, Caco-2
miR-34a↑, curcumin and AKBA induced upregulation of tumor-suppressive miR-34a and downregulation of miR-27a in CRC cells
miR-27a-3p↓,
TumCG↓,
BAX↑,
Bcl-2↓,
PARP1↓,
TumCCA↑,
Apoptosis↑,
cMyc↓,
CDK4↓,
CDK6↓,
cycD1↓,
ChemoSen↑, combined treatment further increased the inhibitory effects
miR-34a↑, miR-34a expression was upregulated by curcumin and further elevated by concurrent treatment with curcumin and AKBA in HCT116 cell
miR-27a-3p↓,

145- CA,  CUR,    The anti-cancer effects of carotenoids and other phytonutrients resides in their combined activity
- in-vitro, NA, NA
AR↓,
ARE/EpRE↑, x4 the sum of single ingredients

2015- CAP,  CUR,  urea,    Anti-cancer Activity of Sustained Release Capsaicin Formulations
- Review, Var, NA
AntiCan↑, Several convergent studies show that capsaicin displays robust cancer activity, suppressing the growth, angiogenesis and metastasis of several human cancers.
TumCG↓,
angioG↓,
TumMeta↓,
BioAv↓, clinical applications of capsaicin as a viable anti-cancer drug have remained problematic due to its poor bioavailability and aqueous solubility properties
BioAv↓, capsaicin is associated with adverse side effects like gastrointestinal cramps, stomach pain, nausea and diarrhea and vomiting
BioAv↑, All these hurdles may be circumvented by encapsulation of capsaicin in sustained release drug delivery systems.
selectivity↑, Most importantly, these long-acting capsaicin formulations selectively kill cancer cells and have minimal growth-suppressive activity on normal cells.
EPR↑, The EPR effect is a mechanism by which high–molecular drug delivery systems (typically prodrugs, liposomes, nanoparticles, and macromolecular drugs) tend to accumulate in tumor tissue much more than they do in normal tissues
eff↓, The efficiency of such extravasation is maximum when the size of the liposomes less than 200 nm The CAP-CUR-GLY-GAL-LIPO were spherical in shape with a narrow range of size distribution ranging from 135–155nm
ChemoSen↑, The chemosensitization and anti-tumor activity of capsaicin involves multiple molecular pathways
Dose∅, oral, Intravenous (IV), and Intraperitoneal (IP) options
Half-Life∅, oral metabolized in 105mins, T1/2in blood=25mins.
eff↑, presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin

428- Chit,  docx,  CUR,    Chitosan-based nanoparticle co-delivery of docetaxel and curcumin ameliorates anti-tumor chemoimmunotherapy in lung cancer
- vitro+vivo, Lung, H460 - vitro+vivo, Lung, H1299 - vitro+vivo, Lung, A549 - vitro+vivo, Lung, PC9
MDSCs↓,
TregCell↓,
IL10↓,
NK cell↑,

469- CUR,    The inhibitory effect of curcumin via fascin suppression through JAK/STAT3 pathway on metastasis and recurrence of ovary cancer cells
- in-vitro, Ovarian, SKOV3
fascin↓,
STAT3↓,
JAK↓,

461- CUR,    Curcumin inhibits prostate cancer progression by regulating the miR-30a-5p/PCLAF axis
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
TumCP↓,
TumCMig↓,
TumCI↓,
Apoptosis↑,
miR-30a-5p↑,
PCLAF↓,
Bcl-2↓,
Casp3↓,
BAX↑,
cl‑Casp3↑,

462- CUR,    Curcumin promotes cancer-associated fibroblasts apoptosis via ROS-mediated endoplasmic reticulum stress
- in-vitro, Pca, PC3
Bcl-2↓,
MMP↓,
cl‑Casp3↑,
BAX↑,
BIM↑,
p‑PARP↑,
PUMA↑,
p‑P53↑,
ROS↑,
p‑ERK↑,
p‑eIF2α↑,
CHOP↑,
ATF4↑,

463- CUR,    Curcumin induces autophagic cell death in human thyroid cancer cells
- in-vitro, Thyroid, K1 - in-vitro, Thyroid, FTC-133 - in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, 8505C
TumAuto↑,
LC3II↑,
Beclin-1↑,
p‑p38↑,
p‑JNK↑,
p‑ERK↑, p-ERK1/2
p62↓,
p‑PDK1↓,
p‑Akt↓,
p‑p70S6↓,
p‑PIK3R1↓,
p‑S6↓,
p‑4E-BP1↓,

464- CUR,    Curcumin inhibits the viability, migration and invasion of papillary thyroid cancer cells by regulating the miR-301a-3p/STAT3 axis
- in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, TPC-1
TumCI↓,
TumCI↓,
MMP2↓,
MMP9↓,
EMT↓,
STAT3↓,
miR-301a-3p↓,
STAT↓,
N-cadherin↓,
Vim↓,
Fibronectin↓,
p‑JAK↓,
p‑JAK2↓,
p‑JAK3↓,
p‑STAT1↓,
p‑STAT2↓,
E-cadherin↑,

465- CUR,    Curcumin inhibits the growth of liver cancer by impairing myeloid-derived suppressor cells in murine tumor tissues
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, HUH7 - vitro+vivo, Liver, MHCC-97H
TumCG↓,
MDSCs↓,
TLR4↓,
NF-kB↓,
IL6↓,
IL1↓, IL-1β
PGE2↓,
COX2↓,
GM-CSF↓,
angioG↓,
VEGF↓,
CD31↓,
GM-CSF↓,
α-SMA↓,
p‑IKKα↓, p-IKKα, p-IKKβ
MyD88↓,

466- CUR,    Curcumin circumvent lactate-induced chemoresistance in hepatic cancer cells through modulation of hydroxycarboxylic acid receptor-1
- in-vitro, Liver, HepG2 - in-vitro, Liver, HuT78
GlucoseCon↓,
lactateProd↓,
pH↑,
NO↑,
LAR↓,
Hif1a↓, gene and protein
LDHA↓,
MCT1↓,
MDR1↓,
STAT3↓,
HCAR1↓,

467- CUR,    Curcumin inhibits liver cancer by inhibiting DAMP molecule HSP70 and TLR4 signaling
- in-vitro, Liver, HepG2
TumCP↓,
TumCI↓,
TumMeta↓,
Apoptosis↑,
HSP70/HSPA5↓,
e-HSP70/HSPA5↓,
TLR4↓,

468- CUR,  5-FU,    Gut microbiota enhances the chemosensitivity of hepatocellular carcinoma to 5-fluorouracil in vivo by increasing curcumin bioavailability
- vitro+vivo, Liver, HepG2 - vitro+vivo, Liver, 402 - vitro+vivo, Liver, Bel7
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
PI3k/Akt/mTOR↓,
p‑PI3K↓,
Bacteria↑, gut microbiota: Lactobacillus, Epsilonbacteraeota, Helicobacterac-eae, Campylobacterales, Helicobacter, Escherichia-shigella, Bifidobacterium, Campylobacteria
cl‑Casp3↑,

458- CUR,    Curcumin suppresses gastric cancer by inhibiting gastrin‐mediated acid secretion
- vitro+vivo, GC, SGC-7901
Casp3↑,
Apoptosis↑,
TumCP↓,

470- CUR,    Regulation of carcinogenesis and modulation through Wnt/β-catenin signaling by curcumin in an ovarian cancer cell line
- in-vitro, Ovarian, SKOV3
Wnt/(β-catenin)↓,
EMT↓,
DNMT3A↓,
cycD1↓,
cMyc↓,
Fibronectin↓,
Vim↓,
E-cadherin↑,
SFRP5↑,

471- CUR,    Curcumin induces apoptotic cell death and protective autophagy by inhibiting AKT/mTOR/p70S6K pathway in human ovarian cancer cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
Apoptosis↑,
TumAuto↑,
p62↓,
p‑Akt↓,
p‑mTOR↓,
p‑P70S6K↓,
Casp9↑,
PARP↑,
ATG3↑,
Beclin-1↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,

472- CUR,    Curcumin inhibits ovarian cancer progression by regulating circ-PLEKHM3/miR-320a/SMG1 axis
- vitro+vivo, Ovarian, SKOV3 - vitro+vivo, Ovarian, A2780S
TumCP↓,
Apoptosis↑,
PCNA↓,
miR-320a↓,
BAX↑,
cl‑Casp3↑,
circ‑PLEKHM3↑,
SMG1↑,

473- CUR,    Curcumin inhibits epithelial-mesenchymal transition in oral cancer cells via c-Met blockade
- in-vitro, Oral, HSC4 - in-vitro, Oral, Ca9-22
Vim↓,
p‑cMET↓,
p‑ERK↓,
pro‑MMP9↓,
E-cadherin↑,

474- CUR,    Modification of radiosensitivity by Curcumin in human pancreatic cancer cell lines
- in-vitro, PC, PANC1 - in-vitro, PC, MIA PaCa-2
TumCD↑,
Apoptosis↑,
DNAdam↑,
γH2AX↑, yH2AX-MFI
TumCCA↑, radiation-sensitive G2/M-phase

475- CUR,    Curcumin induces apoptotic cell death in human pancreatic cancer cells via the miR-340/XIAP signaling pathway
- in-vitro, PC, PANC1
Apoptosis↑,
cl‑Casp3↑,
miR-340↑,
cl‑PARP↑,
XIAP↓,

476- CUR,    The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer
- in-vitro, PC, PATU-8988 - in-vitro, PC, PANC1
TumCMig↓,
TumCI↓,
Apoptosis↑,
NEDD9↓,
p‑Akt↓,
p‑mTOR↓,
PTEN↑,
p73↑,
β-TRCP↑,

477- CUR,    Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells
- in-vitro, Cerv, SiHa
TumCP↓,
TumCCA↑, Inducing G2/M cell cycle arrest
Apoptosis↑,
TumAuto↑,
CycB↓, cyclins B1
CDC25↓,
ROS↑,
p62↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,
cl‑Casp3↑,
cl‑PARP↑,
P53↑,
P21↑,

478- CUR,    Curcumin decreases epithelial‑mesenchymal transition by a Pirin‑dependent mechanism in cervical cancer cells
- in-vitro, Cerv, SiHa
EMT↓,
N-cadherin↓,
Vim↓,
Slug↓,
Zeb1↓,
PIR↓,
Pirin↓,
E-cadherin↑,

449- CUR,    Curcumin Suppresses the Colon Cancer Proliferation by Inhibiting Wnt/β-Catenin Pathways via miR-130a
- vitro+vivo, CRC, SW480
TumCP↓,
β-catenin/ZEB1↓,
TCF↓, TCF4
miR-21↓,
NKD2↑,
miR-130a↓, main target affecting others

438- CUR,    Curcumin Reduces Colorectal Cancer Cell Proliferation and Migration and Slows In Vivo Growth of Liver Metastases in Rats
- vitro+vivo, CRC, CC531
TumCP↓, >30% 48hr
TumVol↓, 5.6 fold
Albumin↑,
ALP↑,
AST↑,
ALAT↑,
cholinesterase↓,

439- CUR,    Curcumin suppresses LGR5(+) colorectal cancer stem cells by inducing autophagy and via repressing TFAP2A-mediated ECM pathway
- in-vitro, CRC, LGR5
Apoptosis↑,
TumAuto↑,
GP1BB↓,
COL9A3↓,
COMP↓,
AGRN↓,
ITGB4↓,
LAMA5↓, curcumin inhibited the extracellular matrix (ECM)-receptor interaction pathway via the downregulation of the following genes: GP1BB, COL9A3, COMP, AGRN, ITGB4, LAMA5, COL2A1, ITGB6, ITGA1, and TNC.
COL2A1↓,
ITGB6↓,
LGR5↓,
TFAP2A↓,
ECM/TCF↓,

440- CUR,    Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells
- vitro+vivo, CRC, SW480 - vitro+vivo, CRC, HT-29
NNMT↓,
p‑STAT3↓,
TumCP↓,
TumCCA↑, G2/M phase cell cycle arrest
ROS↑,

441- CUR,    Curcumin Regulates ERCC1 Expression and Enhances Oxaliplatin Sensitivity in Resistant Colorectal Cancer Cells through Its Effects on miR-409-3p
- in-vitro, CRC, HCT116
ERCC1↓,
Bcl-2↓,
GSTP1/GSTπ↓,
MRP↓,
P-gp↓,
miR-409-3p↑,
survivin↓,

442- CUR,  5-FU,    Curcumin may reverse 5-fluorouracil resistance on colonic cancer cells by regulating TET1-NKD-Wnt signal pathway to inhibit the EMT progress
- in-vitro, CRC, HCT116
Apoptosis↑,
TumCP↓,
TumCCA↑, block of G0/G1 phase
TET1↑,
NKD2↑,
Wnt↓,
EMT↓,
Vim↑,
E-cadherin↓,
β-catenin/ZEB1↓,
TCF↓, TCF4
AXIN1↓, Axin

9- CUR,    Curcumin Suppresses Malignant Glioma Cells Growth and Induces Apoptosis by Inhibition of SHH/GLI1 Signaling Pathway in Vitro and Vivo
- vitro+vivo, MG, U87MG - vitro+vivo, MG, T98G
HH↓,
Shh↓,
Gli1↓,
cycD1↓,
Bcl-2↓,
Foxm1↓,
Bax:Bcl2↑,

444- CUR,  Cisplatin,    LncRNA KCNQ1OT1 is a key factor in the reversal effect of curcumin on cisplatin resistance in the colorectal cancer cells
- vitro+vivo, CRC, HCT8
TumVol↓,
Apoptosis↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑,
cl‑Casp3↑,
cl‑PARP1↑,
miR-497↑,
KCNQ1OT1↓, acts as sponge of miR-497

445- CUR,    Curcumin Regulates the Progression of Colorectal Cancer via LncRNA NBR2/AMPK Pathway
- in-vitro, CRC, HCT116 - in-vitro, CRC, HCT8 - in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
p‑AMPK↑,
p‑ACC-α↑,
NBR2↑,
p‑S6K↓,
mTOR↓,

446- CUR,    The Influence of Curcumin on the Downregulation of MYC, Insulin and IGF-1 Receptors: A Possible Mechanism Underlying the Anti-Growth and Anti-Migration in Chemoresistant Colorectal Cancer Cells
- in-vitro, CRC, SW480
IR↓,
IGF-1↓,
Myc↓,
TumCMig↓,
TumCP↓,

447- CUR,  OXA,    Curcumin reverses oxaliplatin resistance in human colorectal cancer via regulation of TGF-β/Smad2/3 signaling pathway
- vitro+vivo, CRC, HCT116
p‑p65↓,
Bcl-2↓,
Casp3↑,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
N-cadherin↓,
TGF-β↓,
E-cadherin↑,
TumVol↓,
TumCMig↓,

448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,

460- CUR,    Curcumin Suppresses microRNA-7641-Mediated Regulation of p16 Expression in Bladder Cancer
- in-vitro, Bladder, T24 - in-vitro, Bladder, TCCSUP - in-vitro, Bladder, J82
miR-7641↓,
p16↑,
Apoptosis↑,
TumCI↓,

450- CUR,    Curcumin may be a potential adjuvant treatment drug for colon cancer by targeting CD44
- in-vitro, CRC, HCT116 - in-vitro, CRC, HCT8
TumCP↓,
TumCMig↓,
CD44↓, also cellular uptake of curcumin was significantly higher in CD44+ colon cancer cells.

451- CUR,    The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer
- vitro+vivo, HNSCC, SCC15 - vitro+vivo, HNSCC, SNU1076 - vitro+vivo, HNSCC, SNU1041
TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

452- CUR,    Curcumin downregulates the PI3K-AKT-mTOR pathway and inhibits growth and progression in head and neck cancer cells
- vitro+vivo, HNSCC, SCC9 - vitro+vivo, HNSCC, FaDu - vitro+vivo, HNSCC, HaCaT
TumCCA↑, arrested cell cycle at phase G2 /M
PI3k/Akt/mTOR↓,
Casp3↑,
EGFR↓, 0.18 fold
EGF↑, Curcumin induced a noticeable increase in the expression of EGF (11.3-fold change)
PRKCG↑, 13.2 fold
p‑Akt↓,
p‑mTOR↓,
RPS6KA1↓, 0.17 fold
EIF4E↓, 0.18 fold
proCasp3↓,

453- CUR,    Cellular uptake and apoptotic properties of gemini curcumin in gastric cancer cells
- in-vitro, GC, AGS
Bcl-2↓,
survivin↓,
BAX↑,
TumCCA↑, Gemini-Cur compound induced G2/M cell cycle arrest

454- CUR,    Curcumin-Induced DNA Demethylation in Human Gastric Cancer Cells Is Mediated by the DNA-Damage Response Pathway
- in-vitro, GC, MGC803
TumCMig↓,
TumCP↓,
ROS↑,
mtDam↑,
DNAdam↑,
Apoptosis↑,
ATR↑,
P21↑,
p‑P53↑,
GADD45A↑,
p‑γH2AX↑,

455- CUR,    Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin
- in-vitro, GC, SGC-7901
Shh↓,
Gli1↓,
Foxm1↓,
β-catenin/ZEB1↓,
TumCMig↓, induced S phase cell cycle arrest
Apoptosis↑,
TumCCA↑,
Wnt↓,
EMT↓,
E-cadherin↑,
Vim↓,

456- CUR,    Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells
- vitro+vivo, GC, SGC-7901
miR-34a↑,
TumCP↓,
TumCMig↓,
TumCI↓,
TumCCA↑, inhibited cell cycle progression in G0/G1-S phase
Bcl-2↓,
CDK4/6↓, CDK4
cycD1↓,

457- CUR,    Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓,
Apoptosis↑,
TumAuto↑,
P53↑,
PI3K↓,
P21↑,
p‑Akt↓,
p‑mTOR↓,
Bcl-2↓,
Bcl-xL↓,
LC3I↓, LC3I
BAX↑,
Beclin-1↑,
cl‑Casp3↑,
cl‑PARP↑,
LC3II↑,
ATG3↑,
ATG5↑,

482- CUR,  PDT,    The Antitumor Effect of Curcumin in Urothelial Cancer Cells Is Enhanced by Light Exposure In Vitro
- in-vitro, Bladder, RT112 - in-vitro, Bladder, UMUC3
Apoptosis↑, cur + light only
TumCG↓,
TumCP↓,

459- CUR,    Curcumin inhibits cell proliferation and motility via suppression of TROP2 in bladder cancer cells
- in-vitro, Bladder, T24 - in-vitro, Bladder, RT4
Trop2↓,
Apoptosis↑,
cycE1↓,
p27↑,
TumCCA↑, curcumin induced G2/M cell cycle arrest

1980- CUR,  Rad,    Thioredoxin reductase-1 (TxnRd1) mediates curcumin-induced radiosensitization of squamous carcinoma cells
- in-vitro, Cerv, HeLa - in-vitro, Laryn, FaDu
selectivity↑, previously demonstrated that curcumin radiosensitizes cervical tumor cells without increasing the cytotoxic effects of radiation on normal human fibroblasts
RadioS↑,
TrxR↓, inhibitory activity of curcumin on the anti-oxidant enzyme Thioredoxin Reductase-1 (TxnRd1) is required for curcumin-mediated radiosensitization of squamous carcinoma cells
ROS↑, induced reactive oxygen species
ERK↑, sustained ERK1/2 activation
Dose∅, Curcumin treatment resulted in a dose-dependent decrease in TxnRd activity with an IC50 of approximately 10 µM in both cell lines
cl‑PARP↑, curcumin induced a robust increase in cleaved PARP

1488- CUR,    Anti-Cancer and Radio-Sensitizing Effects of Curcumin in Nasopharyngeal Carcinoma
RadioS↑,
ChemoSen↑,

1505- CUR,    Epigenetic targets of bioactive dietary components for cancer prevention and therapy
- Review, NA, NA
TumCCA↑,
Apoptosis↑,
DNMTs↓, curcumin also inhibits DNMT activities and histone modification such as HDAC inhibition in tumorigenesis
HDAC↓,
HATs↓, inhibitory activity against HDACs and HATs in several in vitro cancer models
TumCP↓,
p300↓, Significant decreases in the amounts of p300, HDAC1, HDAC3, and HDAC8
HDAC1↓,
HDAC3↓,
HDAC8↓,
NF-kB↓, inhibition of nuclear translocation of the NF-κB/p65 subunit

1510- CUR,  Chemo,    Combination therapy in combating cancer
- Review, NA, NA
*NRF2↑, Curcuminoids are linear diarylheptanoids that upregulate Nrf2 expression and induce Nrf2 translocation to the nucleus to elicit its antioxidant effects
*GSH↑, curcuminoids upregulate glutathione levels which have been shown to reduce ROS levels and remove carcinogens, aiding in chemoprevention
*ROS↓,
ChemoSideEff↓, aiding in chemoprevention
eff↑, Curcuminoids in combination with chemotherapy have demonstrated an overall positive outcome, and have also shown to increase the survival rate in some patients
OS↓, shown to increase the survival rate in some patients
chemoP↑, have been shown to reduce ROS levels and remove carcinogens, aiding in chemoprevention

1609- CUR,  EA,    Curcumin and Ellagic acid synergistically induce ROS generation, DNA damage, p53 accumulation and apoptosis in HeLa cervical carcinoma cells
- in-vitro, Cerv, NA
eff↑, combination of Curcumin and Ellagic acid at various concentrations showed better anticancer properties than either of the drug when used alone as evidenced by MTT assay
Dose∅, IC50 value for Curcumin is calculated as 16.52 mM and for Ellagic acid the IC50 Value is 19.47 mM. The combination of Curcumin and Ellagic acid has IC50 value 10.9 mM.
ROS↑, Curcumin alone increases the ROS level significantly. Similarly the C + E treated cells exhibited a very high magnitude of ROS level.
DNAdam↑, Curcumin and Ellagic acid show mild degree of DNA damage at this concentration but the C + E treated cells shows greater degree of DNA damage
P53↑, C + E treated cells show greater degree of stabilization of p53
P21↑, Elevated expression of p21 in response to Curcumin and C + E treatment
BAX↑, But the C + E treated cells showed higher expression of Bax
Dose∅, Curcumin daily shows detectable levels of Curcumin in plasma and urine and the concentration is close to 11.1 nMol/l

1616- CUR,  EA,    Kinetics of Inhibition of Monoamine Oxidase Using Curcumin and Ellagic Acid
- in-vitro, Nor, NA
*MAOA↓, MAO activity was inhibited by curcumin and ellagic acid
*Dose∅, however, higher half maximal inhibitory concentrations of curcumin (500.46 nM) and ellagic acid (412.24 nM)
Dose?, MAO-B by curcumin (IC50 500.46 nM) and ellagic acid (IC50 412.24 nM)

1792- CUR,  LEC,    Chondroprotective effect of curcumin and lecithin complex in human chondrocytes stimulated by IL-1β via an anti-inflammatory mechanism
- in-vitro, Arthritis, RAW264.7 - NA, NA, HCC-38
*Inflam↓, curcumin is well known to regulate anti-inflammatory effects, primarily through the deactivation of NF-κB
*NF-kB↓,
*iNOS↓, 10 and 20 μM, complex also suppressed iNOS and COX-2 mRNA expression and inhibited NO and PGE2 production
*COX2↓,
*NO↓,
*PGE2↓,
*MMPs↑, 10 and 20 μM of the complex (Fig. 2A, B, and C). IL-1β noticeably upregulated the production of MMP-1, 2, 3, 9, and 13 and TIMP-1 compared to the control group
*TIMP1↑,
*BioEnh↑, In this study, the complex of curcumin and lecithin enhanced bioavailability of curcumin resulting in chondroprotective effect at relatively lower concentrations.

1809- CUR,  Oxy,    Long-term stabilisation of myeloma with curcumin
- Case Report, Melanoma, NA
*OS↑, plateaued and has remained stable for the last 5 years with good quality of life.
QoL↑, may help to improve quality of life,
Dose↑, few months later, she also embarked on a once-weekly course of hyperbaric oxygen therapy (90 min at 2 ATA) which she has maintained ever since.
Dose↑, oral curcumin complexed with bioperine (to aid absorption), as a single dose of 8 g each evening on an empty stomach.
IL6↓, curcumin prevents myeloma cell proliferation through inhibition of IL-6-induced STAT-3 phosphorylation
STAT3↓, curcumin downregulated the expression of NFkB, COX-2 and STAT3
NF-kB↓,
COX2↓,

1977- CUR,    Synthesis and evaluation of curcumin analogues as potential thioredoxin reductase inhibitors
- in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
TrxR↓, found that most of the analogues can inhibit TrxR in the low micromolar range
Dose↝, TrxR activity in cell lysates declined by approximately 30% after the exposure of HeLa cells to 50 uM of 4g. Similar findings were observed in 4g treated MCF-7 cells
eff↑, showed that analogues 2a, 2e, 2g, and 4g, which turned out to be potent inhibitors of TrxR, exhibited stronger toxicity to A549/R cells than that of the natural curcumin

1978- CUR,    Curcumin targeting the thioredoxin system elevates oxidative stress in HeLa cells
- in-vitro, Cerv, HeLa
TrxR1↓, curcumin can target the cytosolic/nuclear thioredoxin system to eventually elevate oxidative stress in HeLa cells
ROS↑,
DNA-PK↑, subsequently induces DNA oxidative damage
eff↑, curcumin-pretreated HeLa cells are more sensitive to oxidative stress
Trx↓, down-regulates Trx1 level and decreases Trx activity in HeLa cells
Trx1↓,

1979- CUR,  Rad,    Dimethoxycurcumin, a metabolically stable analogue of curcumin enhances the radiosensitivity of cancer cells: Possible involvement of ROS and thioredoxin reductase
- in-vitro, Lung, A549
eff↑, As compared to its parent molecule curcumin, DIMC showed a very potent radiosensitizing effect as seen by clonogenic survival assay.
ROS↑, significant increase in cellular ROS
GSH/GSSG↓, decrease in GSH to GSSG ratio
TrxR↓, inhibition of thioredoxin reductase enzyme by DIMC
selectivity↑, DIMC can synergistically enhance the cancer cell killing when combined with radiation by targeting thioredoxin system.

1487- CUR,    Relationship and interactions of curcumin with radiation therapy
- Review, Var, NA
RadioS↑,
ChemoSen↑,

1981- CUR,    Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- in-vitro, Lung, NA
eff↑, Mitocurcumin, showed 25-50 fold higher efficacy in killing lung cancer cells as compared to curcumin
ROS↑, Mitocurcumin increased the mitochondrial reactive oxygen species (ROS
mt-GSH↓, decreased the mitochondrial glutathione levels
Bax:Bcl2↑, increased BAX to BCL-2 ratio
Cyt‑c↑, cytochrome C release into the cytosol
MMP↓, loss of mitochondrial membrane potential
Casp3↑, increased caspase-3 activity
Trx2↓, mitocurcumin revealed that it binds to the active site of the mitochondrial thioredoxin reductase (TrxR2) with high affinity
TrxR↓, In corroboration with the above finding, mitocurcumin decreased TrxR activity in cell free as well as the cellular system.
mt-DNAdam↑, mitochondrial DNA damage

1982- CUR,    Inhibition of thioredoxin reductase by curcumin analogs
- in-vitro, NA, NA
eff↑, Curcumin analogs were first investigated for their inhibitory effects on thioredoxin reductase (TrxR). Most of them were more potent TrxR inhibitors than natural curcumin.
TrxR↓,

2304- CUR,    Curcumin decreases Warburg effect in cancer cells by down-regulating pyruvate kinase M2 via mTOR-HIF1α inhibition
- in-vitro, Lung, H1299 - in-vitro, BC, MCF-7 - in-vitro, Cerv, HeLa - in-vitro, Pca, PC3 - in-vitro, Nor, HEK293
Glycolysis↓, curcumin inhibits glucose uptake and lactate production (Warburg effect) in a variety of cancer cell lines
GlucoseCon↓,
lactateProd↓,
PKM2↓, by down-regulating PKM2 expression, via inhibition of mTOR-HIF1α axis.
mTOR↓,
Hif1a↓,
selectivity↑, however, no appreciable decrease in Warburg effect was observed in HEK 293 cells
Dose↝, Dose-dependent decrease in Warburg effect started at 2.5 μM with maximal decrease at 20 μM curcumin.
tumCV↓, Curcumin decreases viability of cancer cells

2305- CUR,    Mitochondrial targeting nano-curcumin for attenuation on PKM2 and FASN
- in-vitro, BC, MCF-7
BioAv↑, This nano-curcumin can readily enter mitochondrion in MCF-7 cancer cells.
PKM2↓, expression of both pyruvate kinase M2 and fatty acid synthase in the MCF-7 cancer cells were noticeably inhibited by CUR@DNA-FeS2-DA
FASN↓,
Glycolysis↓,

2307- CUR,    Cell-Type Specific Metabolic Response of Cancer Cells to Curcumin
- in-vitro, Colon, HT29 - in-vitro, Laryn, FaDu
PKM2↓, Siddiqui et al. have recently reported that curcumin downregulates PKM2 expression in cancer cells, consequently decreasing the Warburg effect.
Warburg↓,
mTOR↓, pKM2 downregulation coincided with the inhibition of the mammalian target of rapamycin (mTOR) pathway and consequential downregulation of hypoxia-inducible factor 1-alpha HIF1α
Hif1a↓,
Glycolysis↓, showed that a decrease of PKM2 (mediated by curcumin or by targeted PKM2 silencing) significantly reduces aerobic glycolysis and is also consequential for cell survival.

2308- CUR,    Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells
- in-vitro, Liver, HepG2
GlucoseCon↓, Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production
lactateProd↓,
ECAR↓,
NO↓,
ROS↑, Curcumin favors the ROS production in HepG2 cells in normal as well as hyperglycemic conditions. ROS production was detected in cancer cells treated with curcumin, or doxorubicin, or their combinations in NG or HG medium for 24 h
HK2↓, HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, tr
PFK1↓,
GAPDH↓,
PKM2↓,
LDHA↓,
FASN↓,
GLUT1↓, Curcumin treatment was able to significantly decrease the expression of GLUT1, HKII, and HIF-1α in HepG2 cells either incubated in NG or HG medium.
MCT1↓,
MCT4↓,
HCAR1↓,
SDH↑, Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition
ChemoSen↑, Curcumin Prevents High Glucose-Induced Chemoresistance
ROS↑, Treatment of cells with doxorubicin in presence of curcumin was found to cooperatively augment the ROS level in cells of both NG and HG groups.
BioAv↑, Curcumin Favors Drug Accumulation in Cancer Cells
P53↑, An increased expression of p53 in curcumin-treated cells can be suggestive of susceptibility towards cytotoxic action of anticancer drugs
NF-kB↓, curcumin has therapeutic benefits in hyperglycemia-associated pathological manifestations and through NF-κB inhibition
pH↑, Curcumin treatment was found to resist the lowering of pH of culture supernatant both in NG as well in HG medium.

2312- CUR,    Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy
- Review, Var, NA
ROS↑,
PKM2↓, ROS accumulation inhibits PKM2

2466- CUR,    Regulatory Effects of Curcumin on Platelets: An Update and Future Directions
- Review, Nor, NA
*AntiAg↑, Several studies have proved the beneficial role of curcumin on platelets . in-vivo study exhibited that curcumin inhibited platelet aggregation in monkeys
*antiOx↑, Curcumin exhibits promising antioxidant activity
*Inflam↓,
*12LOX↑, increased the production of 12-LOX
COX1↓, Curcuminoids have been demonstrated to inhibit cyclo-oxygenase and 12-lipoxygenase activities in human platelets, thus showing antioxidant activity
COX2↓, Its effectiveness in cancer is mediated by inhibition of COX-2, MMP-9, and NF-kB
MMP9↓,
NF-kB↓,

2579- CUR,  ART/DHA,    Curcumin-Artemisinin Combination Therapy for Malaria
- in-vivo, NA, NA
OS↑, oral regimen of curcumin with a single injection of α,β-arteether at 750 μg or 1.5 mg per infected mouse led to complete protection of animals against recrudescence and 100% survival
toxicity↓, Curcumin is tolerated at very high doses, and as much as 8 g/day has been given for 3 months to cancer patients on trial without toxic side effects (1)

2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, ROS induction has been implicated as one of the mechanisms of the anticancer activity of curcumin and its derivatives in various cancers
Catalase↓, Curcumin induces ROS by inhibiting the activity of various ROS-related metabolic enzymes, such as CAT, SOD1, glyoxalase 1, and NAD(P)H dehydrogenase [quinone] 1 [146,149]
SOD1↓,
GLO-I↓,
NADPH↓,
TumCCA↑, ROS accumulation further mediates G1 or G2/M cell cycle arrest [146,147,150,154], senescence [146], and apoptosis.
Apoptosis↑,
Akt↓, downregulation of AKT phosphorylation [145
ER Stress↑, endoplasmic reticulum stress (namely through the PERK–ATF4–CHOP axis)
JNK↑, activation of the JNK pathway [151],
STAT3↓, and inhibition of STAT3 [155].
BioAv↑, Additionally, the combination of curcumin and piperine, a pro-oxidative phytochemical that drastically increases the bioavailability of curcumin in humans

1034- CUR,  immuno,    Enhanced anti‐tumor effects of the PD‐1 blockade combined with a highly absorptive form of curcumin targeting STAT3
- in-vivo, NA, NA
DCells↑,
T-Cell↑,

480- CUR,    Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells
- in-vitro, GBM, SNB19
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, G2/M phase
NEDD9↓,
NOTCH1↓,
p‑Akt↓,

481- CUR,  CHr,  Api,    Flavonoid-induced glutathione depletion: Potential implications for cancer treatment
- in-vitro, Liver, A549 - in-vitro, Pca, PC3 - in-vitro, AML, HL-60
GSH↓, depletion
mtDam↑, mitochondrial dysfunction
MMP↓,
Cyt‑c↑,

443- CUR,    Reduced Caudal Type Homeobox 2 (CDX2) Promoter Methylation Is Associated with Curcumin’s Suppressive Effects on Epithelial-Mesenchymal Transition in Colorectal Cancer Cells
- in-vitro, CRC, SW480
DNMT1↓,
DNMT3A↓,
N-cadherin↓,
Vim↓,
Wnt↓, Wnt3a
Snail↓, Snail1
Twist↓,
β-catenin/ZEB1↓,
E-cadherin↑,
EMT↓, Curcumin incubation inhibited EMT
CDX2↓,

483- CUR,  PDT,    Visible light and/or UVA offer a strong amplification of the anti-tumor effect of curcumin
- in-vivo, NA, A431
TumVol↓,
TumCP↓,
Apoptosis↑,

484- CUR,  PDT,    Low concentrations of curcumin induce growth arrest and apoptosis in skin keratinocytes only in combination with UVA or visible light
- in-vitro, Melanoma, NA
Cyt‑c↑, release of cytochrome c from mitochondria
Casp9↑,
Casp8↑,
NF-kB↓,
EGFR↓,

485- CUR,  PDT,    Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin
- in-vitro, Melanoma, NA
NF-kB↓,
Casp8↑,
Casp9↑,
p‑Akt↓,
p‑ERK↓,

872- CUR,  RES,    New Insights into Curcumin- and Resveratrol-Mediated Anti-Cancer Effects
- in-vitro, BC, TUBO - in-vitro, BC, SALTO
TumCP↓,
tumCV↓,
p62↓, reduced by Cur
p62↑, accumulated by Res
TumAuto↑, Cur only
TumAuto↓, Res only
ROS↑, increased ROS with Res
ROS↓, decreased ROS with Cur or combination
CHOP↑, strongly upregulated by the curcumin/resveratrol combination

933- CUR,  EP,    Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study
- in-vitro, BC, NA
Apoptosis↑,
ALDOA↓,
ENO2↓,
LDHA↓, LDH inhibitor
LDHB↓,
PFKP↓,
PGK1↓,
PGM1↓,
PGAM1↓,
OXPHOS↑, upregulation of 10 oxidative phosphorylation pathway proteins
TCA↑, upregulation of 8 tricarboxylic acid (TCA) cycle proteins

990- CUR,    Curcumin inhibits aerobic glycolysis and induces mitochondrial-mediated apoptosis through hexokinase II in human colorectal cancer cells in vitro
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT-29
HK2↓,
Glycolysis↓,
Apoptosis↑,

1006- CUR,    The effect of Curcuma longa extract and its active component (curcumin) on gene expression profiles of lipid metabolism pathway in liver cancer cell line (HepG2)
- in-vitro, Liver, HepG2
TumCP↓,
PGC1A↑,
CPT1A↑,
ACOX1↑,
SCD1↓,
SREBF2↓,
DGAT1↓,

479- CUR,    Curcumin Has Anti-Proliferative and Pro-Apoptotic Effects on Tongue Cancer in vitro: A Study with Bioinformatics Analysis and in vitro Experiments
- in-vitro, Tong, CAL27
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, S-phase cell cycle arrest
Bcl-2↓,
BAX↑,
cl‑Casp3↑,

1108- CUR,    Curcumin: a potent agent to reverse epithelial-to-mesenchymal transition
- Review, NA, NA
EMT↓, inhibition and reversal of the EMT

1383- CUR,  BBR,  RES,    Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases
- Review, NA, NA
GSK‐3β↝,
ROS↑, BBB increased ROS production by decreasing c-MYC expression

1408- CUR,    Antiproliferative and ROS Regulation Activity of Photoluminescent Curcumin-Derived Nanodots
- in-vitro, Lung, A549
ROS↓, antioxidation activity at low concentrations (<0.08 mg/mL) with low levels of reactive oxygen species (ROS) generation, i.e., 82% of the ROS level in cells without treatment for A549 cells;
ROS↑, at high concentrations, the nanodots exhibit a pro-oxidant effect on both the cancer cells (A549) and normal cells (EA.hy926) by inducing more ROS generation and dose-dependent cytotoxicity.

1409- CUR,    Curcumin analog WZ26 induces ROS and cell death via inhibition of STAT3 in cholangiocarcinoma
- in-vivo, CCA, Walker256
TumCG↓,
ROS↑,
MMP↓,
STAT3↓,
TumCCA↑, G2/M cell cycle
eff↓, Pretreatment of N-acetyl cysteine (NAC), an antioxidant agent, could fully reverse the WZ26-induced ROS-mediated changes in CCA cells

1410- CUR,    Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway
- vitro+vivo, OS, MG63
tumCV↓,
Apoptosis↑,
TumCG↓,
NRF2↓, after treatment with curcumin, Nrf2 and GPX4 levels were significantly decreased
GPx4↓,
HO-1↓,
xCT↓, SLC7A11
ROS↑, our results revealed that after treatment with curcumin, ROS and MDA levels were significantly increased while GSH levels were decreased
MDA↑,
GSH↓,

1411- CUR,  Cisplatin,    Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects
- Review, Var, NA
ChemoSen↑, decreasing CP's adverse impacts and improving its antitumor
*ROS↓, Curcumin administration reduces ROS levels to prevent apoptosis in normal cells.
*NF-kB↓, curcumin can inhibit inflammation via down-regulation of NF-κB to maintain the normal function of organs.
TumCCA↑,

1418- CUR,    Potential complementary and/or synergistic effects of curcumin and boswellic acids for management of osteoarthritis
- Review, Arthritis, NA
*COX2↓, Curcumin downregulates the cyclooxygenase-2 (COX-2) pathway, reducing the production of prostaglandins associated with inflammation
*Inflam↓,
*5LO↓, directly inhibits lipoxygenase (LOX)
*NO↓,
*NF-kB↓,
*TNF-α↓,
*IL1↓,
*IL2↑,
*IL6↓,
*IL8↓,
*IL12↓,
*MCP1↓,
*PGE2↓,
*MMP2↓,
*MMP3↓,
*MMP9↓,
*NLRP3↓,
*ROS↓, arthritis(basically normal cell)

1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,

1486- CUR,    Curcumin and lung cancer--a review
- Review, Lung, NA
RadioS↑,
ChemoSen↑,

144- CUR,  Bical,    Combination of curcumin and bicalutamide enhanced the growth inhibition of androgen-independent prostate cancer cells through SAPK/JNK and MEK/ERK1/2-mediated targeting NF-κB/p65 and MUC1-C
- in-vitro, Pca, PC3 - in-vitro, NA, DU145 - in-vitro, NA, LNCaP
p‑ERK↑, ERK1/2
p‑JNK↓, phosphorylation
MUC1↓, MUC1-C protein expression
p65↓,

132- CUR,    Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells
- in-vitro, Pca, NA
TumCCA↑,
ROS↑,
TumAuto↑,
UPR↑,

133- CUR,    Curcumin inhibits prostate cancer by targeting PGK1 in the FOXD3/miR-143 axis
- in-vitro, Pca, NA
miR-143↑,
PDK1↓,
FOXD3↑, upregulated by miR-143

134- CUR,  RES,  MEL,  SIL,    Thioredoxin 1 modulates apoptosis induced by bioactive compounds in prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Apoptosis↑,
ROS↑,
Trx1↓,

135- CUR,    Curcumin induces apoptosis and protective autophagy in castration-resistant prostate cancer cells through iron chelation
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
TfR1/CD71↑,
IRP1↑,

136- CUR,  docx,    Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
BAX↑,
BID↑,
PARP↑,
NF-kB↓,
CDK1↓,
COX2↓,
RTK-RAS↓,
PI3K/Akt↓,
EGFR↓,
HER2/EBBR2↓,
P53↑,

137- CUR,    Curcumin induces G0/G1 arrest and apoptosis in hormone independent prostate cancer DU-145 cells by down regulating Notch signaling
- in-vitro, Pca, DU145
NOTCH1↓,
cycD1↓,
CDK2↓,
P21↑,
p27↑,
P53↑,
Bcl-2↓,
Casp3↑,
Casp9↑,

140- CUR,    Curcumin inhibits cancer-associated fibroblast-driven prostate cancer invasion through MAOA/mTOR/HIF-1α signaling
- in-vitro, Pca, PC3
CAFs/TAFs↓,
EMT↓,
ROS↓, We found that curcumin abolished the CAF-derived CM-induced ROS production and CXCR4 and IL-6 receptor expression in PC3 cells
CXCR4↓,
IL6↓,
MAOA↓,
mTOR↓,
HIF-1↓,

141- CUR,    Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer
- in-vivo, Pca, PC3
BAX↑,
Bcl-2↓,

142- CUR,    Effect of curcumin on the interaction between androgen receptor and Wnt/β-catenin in LNCaP xenografts
- in-vivo, Pca, LNCaP
AR↓, both the mRNA and protein level
PSA↓,

143- CUR,    Nonautophagic cytoplasmic vacuolation death induction in human PC-3M prostate cancer by curcumin through reactive oxygen species -mediated endoplasmic reticulum stress
- in-vitro, Pca, LNCaP - in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ER Stress↑,
CHOP↑,
GRP78/BiP↑,
ROS↑,

131- CUR,    Modulation of AKR1C2 by curcumin decreases testosterone production in prostate cancer
- vitro+vivo, Pca, LNCaP - vitro+vivo, Pca, 22Rv1
AKR1C2↓,
CYP11A1↓,
HSD3B↓,
DHT↓,
testos↓,
StAR↓,
SRD5A1↑,

146- CUR,  EGCG,    Synergistic effect of curcumin on epigallocatechin gallate-induced anticancer action in PC3 prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, DU145
P21↑, protein expression

151- CUR,    Curcumin analogues with high activity for inhibiting human prostate cancer cell growth and androgen receptor activation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, LNCaP
AR↓, cum analog

152- CUR,    Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer
- in-vivo, Pca, NA
β-catenin/ZEB1↓,
AR↓,
STAT3↓,
p‑Akt↓,
Mcl-1↓,
Bcl-xL↓,
cl‑PARP↑, cleavage
miR-21↓,
miR-205↑,

153- CUR,    Curcumin Inhibits Prostate Cancer Bone Metastasis by Up-Regulating Bone Morphogenic Protein-7 in Vivo
- in-vivo, Pca, C4-2B
PSA↓,
TGF-β↓,
BMPs↑, BMP2,7

154- CUR,    Curcumin inhibits expression of inhibitor of DNA binding 1 in PC3 cells and xenografts
- vitro+vivo, Pca, PC3
Id1↓,

155- CUR,    Osteopontin and MMP9: Associations with VEGF Expression/Secretion and Angiogenesis in PC3 Prostate Cancer Cells
- in-vitro, Pca, PC3
p‑ERK↓, ERK1/2
VEGF↓,
angioS↑,

157- CUR,    Curcumin induces cell cycle arrest and apoptosis of prostate cancer cells by regulating the expression of IkappaBalpha, c-Jun and androgen receptor
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
cJun↓,
AR↓,

158- CUR,    Curcumin-targeting pericellular serine protease matriptase role in suppression of prostate cancer cell invasion, tumor growth, and metastasis
- vitro+vivo, Pca, LNCaP
MMP9↓,
Matr↓,

159- CUR,    Crosstalk from survival to necrotic death coexists in DU-145 cells by curcumin treatment
- in-vitro, Pca, DU145
ROS↑, at higher concentrations
p‑Jun↑, phosphorylation
p‑p38↑, phosphorylation

121- CUR,    Screening for Circulating Tumour Cells Allows Early Detection of Cancer and Monitoring of Treatment Effectiveness: An Observational Study
- in-vivo, Pca, NA
CTC↓,

10- CUR,    Curcumin Suppresses Lung Cancer Stem Cells via Inhibiting Wnt/β-catenin and Sonic Hedgehog Pathways
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
HH↓,
Wnt/(β-catenin)↓,
Shh↓,
Smo↓,
Gli1↝,
GLI2↝,

11- CUR,    Curcumin inhibits hypoxia-induced epithelial‑mesenchymal transition in pancreatic cancer cells via suppression of the hedgehog signaling pathway
- in-vitro, PC, PANC1
HH↓,
Shh↓,
Smo↓,
Gli1↓,
N-cadherin↓,
E-cadherin↑,
Vim↓,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓,
Shh↓,
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓,
survivin↓,

13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

14- CUR,    Curcumin, a Dietary Component, Has Anticancer, Chemosensitization, and Radiosensitization Effects by Down-regulating the MDM2 Oncogene through the PI3K/mTOR/ETS2 Pathway
- vitro+vivo, Pca, PC3
PI3K/mTOR/ETS2↓, Curcumin inhibited PI3K activity, as manifested by changes in the phosphorylation status of Akt
MDM2↓,
P21↑,

15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
NF-kB↝,
Akt↝,
AR↝,
Apoptosis↝,
Bcl-2↝,
Casp3↝,
BAX↝,
P21↝,
ROS↝,
Apoptosis↝,
Bcl-xL↝,
JNK↝,
MMP2↝,
P53↝,
PSA↝,
VEGF↝,
COX2↝,
cycD1↝,
EGFR↝,
IL6↝,
β-catenin/ZEB1↝,
mTOR↝,
NRF2↝,
p‑Akt↝,
AP-1↝,
Cyt‑c↝,
PI3K↝,
PTEN↝,
Cyc↝,
TNF-α↝,

117- CUR,    Increased Intracellular Reactive Oxygen Species Mediates the Anti-Cancer Effects of WZ35 via Activating Mitochondrial Apoptosis Pathway in Prostate Cancer Cells
- in-vivo, Pca, RM-1 - in-vivo, Pca, DU145
ROS↑,

118- CUR,    Curcumin analog WZ35 induced cell death via ROS-dependent ER stress and G2/M cell cycle arrest in human prostate cancer cells
- in-vitro, Pca, PC3 - in-vitro, Pca, DU145
ROS↑,
Bcl-2↓,
PARP↑,
cDC2↓,
CycB↓,
MDM2↓,

120- CUR,    A randomized, double-blind, placebo-controlled trial to evaluate the role of curcumin in prostate cancer patients with intermittent androgen deprivation
- Human, Pca, NA
PSA↓,

436- CUR,    Integrated microRNA and gene expression profiling reveals the crucial miRNAs in curcumin anti‐lung cancer cell invasion
- in-vitro, Lung, A549
miR-25-5p↓,
miR-330-5p↑,
MAPK↓,
Wnt↓,

122- CUR,  isoFl,    Combined inhibitory effects of soy isoflavones and curcumin on the production of prostate-specific antigen
- Human, Pca, LNCaP
PSA↓,
AR↓,

123- CUR,    Synthesis of novel 4-Boc-piperidone chalcones and evaluation of their cytotoxic activity against highly-metastatic cancer cells
- in-vitro, Colon, LoVo - in-vitro, Colon, COLO205 - in-vitro, Pca, PC3 - in-vitro, Pca, 22Rv1
NF-kB↓, curcumin analog

124- CUR,    Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, C4-2B
TGF-β↓,
Wnt↓,
PI3k/Akt/mTOR↓,
NF-kB↓,
PTEN↑,
Apoptosis↑,

125- CUR,    Bioactivity of Curcumin on the Cytochrome P450 Enzymes of the Steroidogenic Pathway
- in-vitro, adrenal, H295R
CYP17A1↓,
CYP19↓,

126- CUR,    Modulation of miR-34a in curcumin-induced antiproliferation of prostate cancer cells
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
miR-34a↑,
β-catenin/ZEB1↓,
cMyc↓,
P21↑,
cycD1↓,
PCNA↓,

127- CUR,    The chromatin remodeling protein BRG1 links ELOVL3 trans-activation to prostate cancer metastasis
- in-vitro, Pca, NA
Elvol3↓,

128- CUR,  RES,    Evaluation of biophysical as well as biochemical potential of curcumin and resveratrol during prostate cancer
- in-vivo, Pca, NA
lipid-P↓,

129- CUR,    Curcumin suppressed the prostate cancer by inhibiting JNK pathways via epigenetic regulation
- vitro+vivo, Pca, LNCaP
JNK↓,

130- CUR,    Maspin Enhances the Anticancer Activity of Curcumin in Hormone-refractory Prostate Cancer Cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
BAD↝,
BAX↝,
eff↑, Maspin can enhance the sensitivity of HRPC cells to curcumin treatment

423- CUR,    Inhibition of TLR4/TRIF/IRF3 Signaling Pathway by Curcumin in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
TLR4↓,
IRF3↓,
IFN-γ↓,
TRIF↓,

406- CUR,    Effect of curcumin on normal and tumor cells: Role of glutathione and bcl-2
- in-vitro, BC, MCF-7 - in-vitro, Hepat, HepG2
GSH↓, depletion
Apoptosis↑,
Bcl-2↓, but not HepG2 cells
cMyc↓,

407- CUR,    Curcumin inhibited growth of human melanoma A375 cells via inciting oxidative stress
- in-vitro, Melanoma, A375
Apoptosis↑,
ROS↑,
GSH↓,
MMP↓, wreaking

160- CUR,    Curcumin inhibits prostate cancer metastasis in vivo by targeting the inflammatory cytokines CXCL1 and -2
CXCc↓, CXCL1,2
IκB↓,
NF-kB↓,
COX2↓,
SPARC↓,
EFEMP↓,

409- CUR,    Curcumin Inhibits Glyoxalase 1—A Possible Link to Its Anti-Inflammatory and Anti-Tumor Activity
- in-vitro, Pca, PC3 - in-vitro, BC, MDA-MB-231
GLO-I↓,
GSH↓, 50uM
ATP↓, mostly >50uM

410- CUR,    Nrf2 depletion enhanced curcumin therapy effect in gastric cancer by inducing the excessive accumulation of ROS
- vitro+vivo, GC, AGS - vitro+vivo, GC, HGC27
ROS↑,
NRF2↑, add knockdown of NRF2 enchances CUR efficacy

411- CUR,    Curcumin inhibits the invasion and metastasis of triple negative breast cancer via Hedgehog/Gli1 signaling pathway
- in-vitro, BC, MDA-MB-231
HH↓,
EMT↓,
Gli1↓,

412- CUR,    Curcumin and Its New Derivatives: Correlation between Cytotoxicity against Breast Cancer Cell Lines, Degradation of PTP1B Phosphatase and ROS Generation
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
ROS↑, 25uM
PTP1B↓,

413- CUR,    Curcumin attenuates lncRNA H19-induced epithelial-mesenchymal transition in tamoxifen-resistant breast cancer cells
- in-vitro, BC, MCF-7
N-cadherin↓,
E-cadherin↑,
H19↓, starts about 10% reduction with 5uM

414- CUR,    Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Ferroptosis↑,
Iron↑,
ROS↑,
lipid-P↑,
MDA↑,
GSH↓,
HO-1↑, Curcumin upregulates a variety of ferroptosis target genes related to redox regulation, especially heme oxygenase-1 (HO-1).
NRF2↑,
GPx↓,
ROS↑,
Iron↑, curcumin caused marked accumulation of intracellular iron
GPx4↓,
HSP70/HSPA5↑,
ATFs↑, ATF4
CHOP↑, DDIT3
MDA↑,
FTL↑, Curcumin upregulated FTL (encoding ferritin light chain), FTH1
FTH1↑,
BACH1↑,
REL↑, v-rel reticuloendotheliosis viral oncogene homolog A
USF1↑,
NFE2L2↑,

415- CUR,    Curcumin inhibits proteasome activity in triple-negative breast cancer cells through regulating p300/miR-142-3p/PSMB5 axis
- vitro+vivo, BC, MDA-MB-231
PSMB5↓,
CT-I↓,
miR-142-3p↑,
EP300↓, P300

417- CUR,    Curcumin inhibits the growth of triple‐negative breast cancer cells by silencing EZH2 and restoring DLC1 expression
- vitro+vivo, BC, MCF-7 - vitro+vivo, BC, MDA-MB-231 - vitro+vivo, BC, MDA-MB-468
EZH2↓,
DLC1↑,
cycA1↓,
CDK1↓,
Bcl-2↓,
Casp9↑,
DLC1↑,

420- CUR,    Anti-metastasis activity of curcumin against breast cancer via the inhibition of stem cell-like properties and EMT
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Vim↓,
Fibronectin↓,
β-catenin/ZEB1↓,
E-cadherin↓,
CD44↑, The CD44+CD24-/low subpopulation was larger in mammospheres when MCF-7 and MDA-MB-231 adherent cells were cultured with SFM.
CD24↓,
OCT4↓,
Nanog↓,
SOX2↓,

422- CUR,    Curcumin induces re-expression of BRCA1 and suppression of γ synuclein by modulating DNA promoter methylation in breast cancer cell lines
- in-vitro, BC, HCC-38 - in-vitro, BC, T47D
BRCA1↑,
TET1↑,
DNMT3A↑, Curcumin downregulates the expression of DNMT1 and upregulates TET1 and DNMT3 in HCC-38 cells
DNMT1↓,
SNCG↓,
miR-29b↓, HCC-38 cells
miR-29b↑, upregulates miR-29b in T47D cells

408- CUR,    Cytotoxic, chemosensitizing and radiosensitizing effects of curcumin based on thioredoxin system inhibition in breast cancer cells: 2D vs. 3D cell culture system
- in-vitro, BC, MCF-7
Trx1↓,

424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓,
p‑STAT1↓, pSTAT-1
p‑Akt↓,
p‑p44↓, p-p44
p‑p42↓, p-p42
RAS↓,
Raf↓, c-RAF
Vim↓,
β-catenin/ZEB1↓,
P53↓,
Bcl-2↓,
Mcl-1↓,
PIAS-3↑,
SOCS-3↑,
SOCS1↑,
ROS↑,
NF-kB↓, NF-kB inactivation, ROS generation and PA depletion in MCF-7, MDA-MB-453 and MDA-MB-231 breast can- cer cells
PAO↑,
SSAT↑,
P21↑,
Bak↑,

425- CUR,    Curcumin inhibits proliferation and promotes apoptosis of breast cancer cells
- in-vitro, BC, T47D - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
CDC25↓,
cDC2↓,
P21↑,
p‑Akt↓,
p‑mTOR↓, phosphorylation
Bcl-2↓,
BAX↑,
Casp3↑,

426- CUR,    Use of cancer chemopreventive phytochemicals as antineoplastic agents
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, CAL51
Bcl-2↓,
ROS↑,
BAX↑,
RAD51↑,
γH2AX↑,

427- CUR,    Curcumin suppresses the malignancy of non-small cell lung cancer by modulating the circ-PRKCA/miR-384/ITGB1 pathway
- in-vitro, Lung, H1299 - in-vitro, Lung, H460 - vitro+vivo, Lung, A549
ITGB1↓,
circ-PRKCA↓,
miR-384↑,

429- CUR,    TAp63α Is Involved in Tobacco Smoke-Induced Lung Cancer EMT and the Anti-cancer Activity of Curcumin via miR-19 Transcriptional Suppression
- in-vitro, Lung, H1299 - in-vitro, Lung, A549
TAp63α↑,
E-cadherin↑,
ZO-1↑,
Vim↓,
N-cadherin↓,
miR-19b↓, miR-19a, miR-19b

430- CUR,    Curcumin suppresses tumor growth of gemcitabine-resistant non-small cell lung cancer by regulating lncRNA-MEG3 and PTEN signaling
- vitro+vivo, Lung, A549
PTEN↑,
MEG3↑,

431- CUR,    Curcumin suppresses the stemness of non-small cell lung cancer cells via promoting the nuclear-cytoplasm translocation of TAZ
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
ALDH1A1↓,
CD133↓,
EpCAM↓,
OCT4↓,
TAZ↓,
Hippo↑,
p‑TAZ↑,

432- CUR,    Curcumin-Induced Global Profiling of Transcriptomes in Small Cell Lung Cancer Cells
- in-vitro, Lung, H446
Bcl-2↓,
cycF↓,
LOX1↓,
VEGF↓, VEGFB
MRGPRF↓,
BAX↑,
Cyt‑c↑,
miR-548ah-5p↑,

433- CUR,    Curcumin Inhibits the Migration and Invasion of Non-Small-Cell Lung Cancer Cells Through Radiation-Induced Suppression of Epithelial-Mesenchymal Transition and Soluble E-Cadherin Expression
- in-vitro, Lung, A549
E-cadherin↓,
Vim↓,
Slug↓,
N-cadherin↓,
Snail↓, N-cadherin and Snail expression showed a slight decrease after treatment with different concentrations of curcumin.
MMP9↓, Curcumin inhibited MMP9 expression
EMT↓, Curcumin inhibits NSCLC migration and invasion by suppressing radiation-induced EMT and sE-cad expression by decreasing MMP9 expression

434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓,
p‑BAD↓, p-Bad
p‑Akt↓,
Akt↓,
cl‑Casp9↑, cleaved
cl‑PARP↑, cleaved

435- CUR,    Antitumor activity of curcumin by modulation of apoptosis and autophagy in human lung cancer A549 cells through inhibiting PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549
Apoptosis↑,
TumAuto↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,
Beclin-1↑,
p62↓,
PI3K↓,
Akt↓,
mTOR↓,
p‑Akt↓,
p‑mTOR↓,
NA↓,

437- CUR,    Anti-cancer activity of amorphous curcumin preparation in patient-derived colorectal cancer organoids
- vitro+vivo, CRC, TCO1 - vitro+vivo, CRC, TCO2
cycD1↓,
cMyc↓,
p‑ERK↓,
CD44↓,
CD133↓,
LGR5↓,
TumCCA↑, proportion of cells in the G0/G1 phase in CRC organoids significantly increased at 24 h
TumVol↓,

161- CUR,  MeSA,    Enhanced apoptotic effects by the combination of curcumin and methylseleninic acid: potential role of Mcl-1 and FAK
- in-vitro, BC, MDA-MB-231 - in-vitro, Pca, DU145
Mcl-1↑, CUR alone
Mcl-1↓, CUR+MeSA
MPT↑,
AIF↑,

165- CUR,    Curcumin interrupts the interaction between the androgen receptor and Wnt/β-catenin signaling pathway in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓,
β-catenin/ZEB1↓,
p‑Akt↓,
GSK‐3β↓,
p‑β-catenin/ZEB1↑, phosphorylated
cycD1↓,
cMyc↓,

167- CUR,    Curcumin-induced apoptosis in PC3 prostate carcinoma cells is caspase-independent and involves cellular ceramide accumulation and damage to mitochondria
- in-vitro, Pca, PC3
MAPK↑,
JNK↑,
Casp3↑,
Casp8↑,
Casp9↑,
AIF↑, released from mitochondria

164- CUR,    Anti-tumor activity of curcumin against androgen-independent prostate cancer cells via inhibition of NF-κB and AP-1 pathway in vitro
- in-vitro, Pca, PC3
NF-kB↓,
AP-1↓,

163- CUR,    Epigenetic CpG Demethylation of the Promoter and Reactivation of the Expression of Neurog1 by Curcumin in Prostate LNCaP Cells
- in-vitro, Pca, LNCaP
MeCP2↓, decreased the MeCP2-Neurog1 binding dramatically
Neurog1↑, our present study provides evidence on the CpG demethylation ability of CUR on Neurog1 while activating its expression
HDAC↓, CUR Treatment Decreases the Total HDAC Activity (50%)

168- CUR,    Curcumin inhibits Akt/mammalian target of rapamycin signaling through protein phosphatase-dependent mechanism
- in-vitro, Pca, PC3
Akt↓,
mTOR↓,
AMPK↑,
TAp63α↑, MAP kinases

169- CUR,    Curcumin inhibits the expression of vascular endothelial growth factor and androgen-independent prostate cancer cell line PC-3 in vitro
- in-vitro, Pca, PC3
VEGF↓,

162- CUR,  EGCG,  SFN,    Shattering the underpinnings of neoplastic architecture in LNCap: synergistic potential of nutraceuticals in dampening PDGFR/EGFR signaling and cellular proliferation
- in-vitro, Pca, LNCaP
p‑PDGF↓, phosphorylation

170- CUR,    Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis and angiogenesis
- vitro+vivo, Pca, PC3
TRAILR↑,
BAX↑,
P21↑,
p27↑,
NF-kB↓,
cycD1↓,
VEGF↓,
uPA↓,
MMP2↓,
MMP9↓,
Bcl-2↓,
Bcl-xL↓,

181- CUR,    The effects of curcumin on the invasiveness of prostate cancer in vitro and in vivo
- vitro+vivo, Pca, DU145
MMP2↓,
MMP9↓,

182- CUR,  RES,  GI,    Chemopreventive anti-inflammatory activities of curcumin and other phytochemicals mediated by MAP kinase phosphatase-5 in prostate cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vitro, Pca, LAPC-4
p38↓,
MKP5↑,

183- CUR,    Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
AR↓,
AP-1↓,
NF-kB↓, The results obtained here demonstrate that curcumin has a potential therapeutic effect on prostate cancer cells through down-regulation of AR and AR-related cofactors (AP-1, NF-kappaB and CBP).
CBP↓,

404- CUR,    Curcumin induces ferroptosis in non-small-cell lung cancer via activating autophagy
- vitro+vivo, Lung, A549 - vitro+vivo, Lung, H1299
TumAuto↑,
TumCG↓,
TumCP↓,
Iron↑, iron overload
GSH↓, GSH depletion
lipid-P↑, accumulation of intracellular iron and lipid‐reactive oxygen species (ROS), lipid peroxidation
GPx↓, GPX4
mtDam↑, mitochondrial membrane rupture
autolysosome↑,
Beclin-1↑,
LC3s↑,
p62↓,
Ferroptosis↑, via activating autophagy

405- CUR,  5-FU,    Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis
- vitro+vivo, CRC, HCT116
Apoptosis↑, more pronounced increase in apoptosis in p53-deficient when compared to p53-proficient cells
TumCMig↓,
NRF2↑,
ROS↑, antioxidant N-acetylcysteine suppressed the induction of apoptosis by curcumin
MET↓,
NA↑,

2976- CUR,    Curcumin suppresses the proliferation of oral squamous cell carcinoma through a specificity protein 1/nuclear factor‑κB‑dependent pathway
- in-vitro, Oral, HSC3 - in-vitro, HNSCC, CAL33
tumCV↓, Cur significantly inhibited the viability and colony formation ability of HSC3 and CAL33 cells.
Sp1/3/4↓, Cur decreased the expression of Sp1, p65 and HSF1 by suppressing their transcription levels.
p65↓,
HSF1↓,
NF-kB↓, Cur decreased NF‑κB activity in OSCC cells, and Sp1 downregulation enhanced the effect of Cur.

3583- CUR,    Curcumin: an orally bioavailable blocker of TNF and other pro-inflammatory biomarkers
- Review, NA, NA
*TNF-α↓, Curcuma longa) that is very inexpensive, orally bioavailable and highly safe in humans, yet can block TNF-α action and production in in vitro models, in animal models and in humans

2977- CUR,    Curcumin Down-Regulates Toll-Like Receptor-2 Gene Expression and Function in Human Cystic Fibrosis Bronchial Epithelial Cells
- in-vitro, CF, NA
*TLR2↓, inhibits TLR2 expression in CF bronchial epithelial cell line, CFBE41o- cells
*Sp1/3/4↓, Interestingly, curcumin treatment decreased nuclear expression of transcription factor specificity protein 1 (SP1),

2978- CUR,    N-acetyl cysteine mitigates curcumin-mediated telomerase inhibition through rescuing of Sp1 reduction in A549 cells
- in-vitro, Lung, A549
ROS↑, ROS induced by curcumin in A549 cells was detected by flow cytometry
hTERT↓, human telomerase reverse transcriptase (hTERT) decreased in the presence of curcumin
Sp1/3/4↓, curcumin decreases the expression of Sp1 through proteasome pathway
eff↓, NAC blunted the Sp1 reduction and hTERT downregulation by curcumin.

2979- CUR,  GB,    Curcumin overcome primary gefitinib resistance in non-small-cell lung cancer cells through inducing autophagy-related cell death
- in-vitro, Lung, H157 - in-vitro, Lung, H1299
EGFR↓, Combination treatment with curcumin and gefitinib markedly downregulated EGFR activity through suppressing Sp1 and blocking interaction of Sp1 and HADC1,
Sp1/3/4↓,
ERK↓, and markedly suppressed receptor tyrosine kinases as well as ERK/MEK and AKT/S6K pathways in the resistant NSCLC cells.
MEK↓,
Akt↓,
S6K↓,

2980- CUR,    Inhibition of NF B and Pancreatic Cancer Cell and Tumor Growth by Curcumin Is Dependent on Specificity Protein Down-regulation
- in-vivo, PC, NA
TumCG↓, curcumin inhibits Panc28 and L3.6pL pancreatic cancer cell and tumor growth in nude mice bearing L3.6pL cells as xenografts
p50↓, curcumin decreased expression of p50 and p65 proteins and NFkappaB-dependent transactivation and also decreased Sp1, Sp3, and Sp4 transcription factor
p65↓,
NF-kB↓,
Sp1/3/4↓,
MMP↓, Curcumin also decreased mitochondrial membrane potential and induced reactive oxygen species in pancreatic cancer cell
ROS↑,

3574- CUR,    The effect of curcumin (turmeric) on Alzheimer's disease: An overview
- Review, AD, NA
*antiOx↑, Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD
*Inflam↓,
*lipid-P↓,
*cognitive↑,
*memory↑, overall memory in patients with AD has improved.
*Aβ↓, curcumin may help the macrophages to clear the amyloid plaques found in Alzheimer's disease.
*COX2↓, Curcumin is found to inhibit cyclooxygenase (COX-2),
*ROS↓, The reduction of the release of ROS by stimulated neutrophils, inhibition of AP-1 and NF-Kappa B inhibit the activation of the pro-inflammatory cytokines TNF (tumor necrosis factor)-alpha and IL (interleukin)-1 beta
*AP-1↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*SOD↑, It also increased the activity of superoxide dismutase, sodium-potassium ATPase that normally decreased with aging.
*GSH↑, followed by a significant elevation in oxidized glutathione content.
*HO-1↑, curcumin induces hemoxygenase activity.
*IronCh↑, curcumin effectively binds to copper, zinc and iron.
*BioAv↓, Curcumin has poor bioavailability. Because curcumin readily conjugated in the intestine and liver to form curcumin glucuronides.
*Half-Life↝, , serum curcumin concentrations peaked one to two hours after an oral dose
*Dose↝, Peak serum concentrations were 0.5, 0.6 and 1.8 micromoles/L at doses of 4, 6 and 8 g/day respectively.
*BBB↑, Curcumin crosses the blood brain barrier and is detected in CSF
*BioAv↑, Absorption appears to be better with food.
*toxicity∅, A phase 1 human trial with 25 subjects using up to 8000 mg of curcumin per day for three months found no toxicity from curcumin.
*eff↑, Co-supplementation with 20 mg of piperine (extracted from black pepper) significantly increase the bioavailablity of curcumin by 2000%

3575- CUR,    The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse
- in-vivo, AD, NA
*antiOx↓, potent polyphenolic antioxidant
*ROS↓, Low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1β, a proinflammatory cytokine elevated in the brains of these mice.
*IL1β↓,
*Aβ↓, low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP was reduced, and insoluble β-amyloid (Aβ), soluble Aβ, and plaque burden were significantly decreased by 43–50%
*Inflam↓, we report that the Indian spice curcumin suppresses indices of inflammation and oxidative damage in the brains of APPSw mice, factors that have been implicated in AD pathogenesis.
*toxicity↓, Studies have consistently shown that curcumin is relatively nontoxic and has few side effects at doses greater than the low dose tested in our mice.

3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments caused marked increase in ChAT positive cells.

3577- CUR,    Oral curcumin for Alzheimer's disease: tolerability and efficacy in a 24-week randomized, double blind, placebo-controlled study
- Trial, AD, NA
*cognitive∅, unable to demonstrate clinical or biochemical evidence of efficacy of Curcumin C3 Complex® in AD in this 24-week placebo-controlled trial although preliminary data suggest limited bioavailability of this compound.
*BioAv↑, The levels of native curcumin measured in plasma were low (7.32 ng/mL).

3578- CUR,  SIL,    Curcumin, but not its degradation products, in combination with silibinin is primarily responsible for the inhibition of colon cancer cell proliferation
- in-vitro, CRC, DLD1
eff↑, combination of curcumin and silymarin exhibited synergistic anticancer activity.
BioAv↓, Despite the low bioavailability of curcumin and the relatively low daily dietary intake (Shen et al. 2016, Teiten et al. 2010, Tsuda 2018), the beneficial effect of curcumin observed could be due to other phytochemicals present in the diet and act sy
TumCG↓, curcumin and silibinin in combination inhibit cell growth significantly

3579- CUR,  SNP,    Metal–Curcumin Complexes in Therapeutics: An Approach to Enhance Pharmacological Effects of Curcumin
- Review, NA, NA
*IronCh↑, It is well established that curcumin strongly chelates several metal ions, including boron, cobalt, copper, gallium, gadolinium, gold, lanthanum, manganese, nickel, iron, palladium, platinum, ruthenium, silver, vanadium, and zinc.
*BioAv↑, Metal–curcumin complexes increase the solubility, cellular uptake, and bioavailability and improve the antioxidant, anti-inflammatory, antimicrobial, and antiviral effects of curcumin.
*antiOx↑,
*Inflam↓,
*BioAv↑, complexes of curcumin with transition metals may provide another approach to overcome the issues associated with curcumin.
ROS↑, curcumin–metal complexes with liposomes present enhanced cellular uptake and ROS generation in cancer cells and thus cause increased cytotoxicity
*neuroP↑, Since curcumin has the ability to cross the blood–brain barrier due to its hydrophobic nature, it can strongly chelate the metal ions in the brain and prevent metal-induced neurotoxicity.
*eff↑, Curcumin with silver nanoparticle formates also increases the solubility and stability of curcumin in complexes. Curcumin reduces and caps the silver nanoparticles, which increases its stability and solubility in water

3580- CUR,    Curcumin Acts as Post-protective Effects on Rat Hippocampal Synaptosomes in a Neuronal Model of Aluminum-Induced Toxicity
- in-vivo, AD, NA
*ROS↓, curcumin post-treatment significantly improved oxidative damage and morphological alterations, and suppressed cytochrome c and caspase 3 activities
*Cyt‑c↓,
*Casp3↓,
*neuroP↑, curcumin had more therapeutic effects than protective effects in AlCI3-induced neurotoxicity.

3581- CUR,    Curcumin Attenuated Neurotoxicity in Sporadic Animal Model of Alzheimer's Disease
- NA, AD, NA
*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓, treatment with CUR enhances pro-oxidant levels, antioxidant enzymes activities and anti-inflammatory cytokine production and decreases apoptotic cells in AlCl3-exposed hippocampus rats.
*BBB↑, CUR is able to cross the blood–brain barrier
*NRF2↑, CUR was shown to provide neuroprotection by inducing the upregulation of the transcription of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and by suppression of NF-κB activation
*NF-kB↓,
*cognitive↑, CUR Protects against AlCl3-Induced Cognitive Impairment
*ROS↓, Co-treatment with CUR significantly attenuated oxidative stress in the hippocampus by decreasing levels of MDA and enhancing SOD and catalase activities, when compared to AlCl3-treated animals.
*MDA↓,
*SOD↑,
*Catalase↑,
*INF-γ↓, CUR significantly reduced INF-γ concentration,
*IL4↓, our results showed that co- and post-treatments of CUR reduce IL-4 concentration.
*memory↑, CUR treatments protect rats against deterioration of spatial memory and
*TNF-α↓, CUR modulated the inflammatory status by the (i) inhibition of TNF-α and IL-1β production in the rat brain
*IL1β↓,

3582- CUR,  PI,    Therapeutic and Preventive Effects of Piperine and its Combination with Curcumin as a Bioenhancer Against Aluminum-Induced Damage in the Astrocyte Cells
*eff↑, In conclusion, the results of the study showed that the use of different concentrations of piperine, curcumin, and their combination had significantly higher % cell viability on aluminum-induced damage in astrocyte cells compared to the damaged contr
*IL6↓, decrease in the amount of IL-6 and TGF-β cytokines also supported that piperine increased the effectiveness of curcumin.
*TGF-β↓,
*BioAv↑, bioavailability-enhancing property of piperine on curcumin was shown for the first time in the literature.

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↓,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

2816- CUR,    NEUROPROTECTIVE EFFECTS OF CURCUMIN
- Review, AD, NA - Review, Park, NA
*neuroP↑, Curcumin has an outstanding safety profile and a number of pleiotropic actions with potential for neuroprotective efficacy, including anti-inflammatory, antioxidant, and anti-protein-aggregate activities.
*Inflam↓,
*antiOx↑,
*BioAv↓, despite concerns about poor oral bioavailability, curcumin has at least 10 known neuroprotective action
*AP-1↓, Curcumin inhibition of AP-1 and NF-κB-mediated transcription occurs at relatively low (<100 nM) doses and might be due to inhibition of histone acetylase (HAT) or activation of histone deacetylase (HDAC) activity
*NF-kB↓,
*HATs↓,
*HDAC↑,
Dose↑, At high doses (>3 µM) that are relevant to colon cancer but unlikely achievable with oral delivery in plasma and tissues outside of the gut, curcumin can act as an alkylating agent,10 a phase II enzyme inducer,11 and stimulate antioxidant response el
*ROS↓, We also found that curcmin reduced oxidative damage, inflammation, and cognitive deficits in rats receiving CNS infusions of toxic Aβ
*cognitive↑,
*Aβ↓, dose-dependently blocked Aβ aggregation at submicromolar concentrations

2808- CUR,    Iron chelation by curcumin suppresses both curcumin-induced autophagy and cell death together with iron overload neoplastic transformation
- in-vitro, Liver, HUH7
Ferritin↓, cells treated with curcumin also exhibit a decrease in ferritin, which is consistent with its chemical structure and iron chelating activity.
IronCh↑,
TumAuto↑, curcumin-induced autophagy and apoptosis, together with the tumorigenic action of iron overload.
Apoptosis↑,
eff↝, The assay of intracellular iron showed that iron chelation by curcumin does not alter cellular iron uptake, whereas curcumin only slightly affected the total amount of intracellular iron
Dose↝, interesting to note that there is a huge difference between 10 and 25 μM curcumin treatment and also that cumulated cell death (apoptosis + necrosis) reached 60–70% at 25 μM curcumin with 24-h incubation.

2809- CUR,    Comparative absorption of curcumin formulations
- in-vivo, Nor, NA
BioAv↑, co-administration of curcumin with an extract obtained from the black pepper has been shown to increase the absorption (AUC) of curcumin by 1.5-fold.
BioAv↑, Whereas, a complex of curcumin with phospholipids increased absorption by 3.4-fold
BioAv↑, and a formulation of curcumin with a micellar surfactant (polysorbate) has been shown to increase the absorption of curcumin in mice 9.0-fold
BioAv↑, A micro emulsion system of curcumin, which consists of Capryol 90 (oil), Cremophor RH40 (surfactant), and Transcutol P aqueous solution (co-surfactant) has been shown to increase the relative absorption in rats by 22.6-fold
BioAv↑, Polylactic-co-glycolic acid (PLGA) and PLGA-polyethylene glycol (PEG) (PLGA-PEG) blend nanoparticles increased curcumin absorption by 15.6- and 55.4-fold, respectively, compared to an aqueous suspension of curcumin in rats
BioAv↓, curcumin are limited by its poor solubility, low absorption from the gut, rapid metabolism and rapid systemic elimination.
Half-Life↝, Our data indicated that the curcumin half-life was estimated to be 6-7 hours

2810- CUR,    Effect of curcuminoids on oxidative stress: A systematic review and meta-analysis of randomized controlled trials
- Review, Nor, NA
*SOD↑, significant increase of SOD activities especially for studies ≥6 weeks
*lipid-P↓, also significantly reduced lipid peroxides, increased GSH and catalase activity.
*GSH↑,
*Catalase↑,
*ROS↓, neutralization of free radicals

2811- CUR,    Effect of Curcumin Supplementation During Radiotherapy on Oxidative Status of Patients with Prostate Cancer: A Double Blinded, Randomized, Placebo-Controlled Study
- Human, Pca, NA
*antiOx↑, Curcumin is an antioxidant agent with both radiosensitizing and radioprotective properties
radioP↑,
RadioS∅, In the present study we have failed to observe any radiosensitizing or prooxidant feature for curcumin in the prescribed dose;
*TAC↑, The present study showed that curcumin can increase TAC and decrease SOD activity in the plasma of patients with prostate cancer receiving radiotherapy; these observations are thought to be possibly brought about by the antioxidant effect of curcumin
*SOD↓,

2812- CUR,    Curcumin Induces High Levels of Topoisomerase I− and II−DNA Complexes in K562 Leukemia Cells
- in-vitro, AML, K562
TOP1↑, this study shows for the first time that curcumin induces topo I and topo II (α and β)−DNA complexes in K562 leukemia cells.
TOP2↑,
eff↓, Curcumin-induced topo I and topo II−DNA complexes were prevented by the antioxidant N-acetylcysteine; this suggests that, unlike the standard topo inhibitors, reactive oxygen species may mediate the formation of these complexes

2813- CUR,    Oxidative Metabolites of Curcumin Poison Human Type II Topoisomerases
- Review, NA, NA
TOP2↑, the dietary spice turmeric enhanced topoisomerase II-mediated DNA cleavage.

2814- CUR,    Curcumin in Cancer and Inflammation: An In-Depth Exploration of Molecular Interactions, Therapeutic Potentials, and the Role in Disease Management
- Review, Var, NA
*BioAv↓, curcumin’s practical application in medicine is hindered by its limited bioavailability. low solubility in water and rapid breakdown in the body
*Inflam↓, anti-inflammatory, antioxidant, and potential anticancer abilities
*antiOx↑,
AntiCan↑,
CK2↓, Curcumin exhibited an IC50 of 2.38 ± 0.15 μM against CK2α
GSK‐3β↓, roles of GSK3β and how they are suppressed by curcumin
EGFR↓, roles of EGFR and how it is inhibited by the curcumin analog, 3a
TOP1↓, unwinding of DNA supercoils by Topo I and Topo II and their inhibition by cyclocurcumin
TOP2↓,
NF-kB↓, The activation of NF-kB signaling and the inhibition of NF-kB’s activity are portrayed in Figure 5.
COX2↓, curcumin itself interacts with COX-2 and potentially inhibits its function
CRP↓, ole of CRP in inducing inflammation and its inhibition by curcumin are depicted in Figure 6.

2815- CUR,    Biochemical and cellular mechanism of protein kinase CK2 inhibition by deceptive curcumin
*CK2↑, ferulic acid was identified as the principal curcumin degradation product responsible for CK2 inhibition

2975- CUR,    Curcumin inhibits proliferation, migration and neointimal formation of vascular smooth muscle via activating miR-22
- in-vivo, Nor, NA
*miR-22↑, Curcumin increased the expression of miR-22 (81%, p < 0.05) and decreased the protein expression of SP1 in VSMCs
*Sp1/3/4↓,

2817- CUR,    Neuroprotection by curcumin: A review on brain delivery strategies
- Review, Nor, NA
*BioAv↝, blood–brain barrier (BBB) is the major obstacle for the delivery of curcumin into the brain, limiting its therapeutic potential.
neuroP↑, Although it appears to possess important neuroprotective properties, the utility of curcumin is limited because of its poor brain bioavailability owing to poor absorption and stability at physiological pH, high rate of metabolism, rapid systemic elim

2818- CUR,    Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways
- Review, AD, NA
*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

2819- CUR,  Chemo,    Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury
- Review, Var, NA
*hepatoP↑, Several studies have shown that curcumin could prevent and/or palliate chemotherapy-induced liver injury
*Inflam↓, mainly due to its anti-inflammatory, antioxidant, antifibrotic and hypolipidemic properties.
*antiOx↓,
*lipid-P↓, Curcumin can lower lipid peroxidation by increasing the content of GSH, a major endogenous antioxidant,
*GSH↑,
*SOD↑, as well as by enhancing the activity of endogenous antioxidant enzymes, such as SOD, CAT, GPx and GST
*Catalase↑,
*GPx↑,
*GSTs↑,
*ROS↓, elimination of ROS
*ALAT↓, attenuated the increase in serum levels of TNF-α as well as several liver enzymes, including ALT, AST, alkaline phosphatase and MDA which are markers of liver damage caused by MTX or cisplatin.
*AST↓,
*MDA↓,
*NRF2↑, Curcumin also attenuated DILI through activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway
*COX2↑, Curcumin can also inhibit the expression of cyclooxygenase-2 (COX-2)
*NF-kB↓, NF-κB inhibition, which decreased the downstream induction of COX-2, ICAM-1 and MCP-1 pro-inflammatory regulators
*ICAM-1↓,
*MCP1↓,
*HO-1↑, increase in HO-1 and NQO1 expression
CXCc↓, Downregulation of pro-inflammatory chemokines, (CXCL1, CXCL2, and MCP-1)

2820- CUR,    Hepatoprotective Effect of Curcumin on Hepatocellular Carcinoma Through Autophagic and Apoptic Pathways
- in-vitro, HCC, HepG2
*hepatoP↑, Curcumin also significantly reduced oxidative stress in liver, inhibited apoptosis, and induced autophagy. In vitro, curcumin (50 μM) decreased HepG2 cells viability and the concentration of SQSTM1.
*ROS?,
tumCV↓,

2821- CUR,    Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)
- Review, Var, NA
*antiOx↑, Curcumin is a plant polyphenol in turmeric root and a potent antioxidant
*NRF2↑, regulation by nuclear factor erythroid 2-related factor 2, thereby suppressing reactive oxygen species (ROS) and exerting anti-inflammatory, anti-infective and other pharmacological effects
*ROS↓,
*Inflam↓,
ROS↑, Of note, curcumin induces oxidative stress in tumors. curcumin-induced accumulation of ROS in tumors to kill tumor cells has been noted in several studies
p‑ERK↑, Curcumin promoted ERK/JNK phosphorylation, causing elevated ROS levels and triggering mitochondria-dependent apoptosis
ER Stress↑, Curcumin triggered disturbances in Ca2+ homeostasis, leading to endoplasmic reticulum stress, mitochondrial damage and apoptosis
mtDam↑,
Apoptosis↑,
Akt↓, Curcumin inhibited the AKT/mTOR/p70S6K signaling pathway
mTOR↓,
HO-1↑, Curcumin-induced HO-1 overexpression led to a disturbed intracellular iron distribution and triggered the Fenton reaction
Fenton↑,
GSH↓, Non-small cell lung cancer: Curcumin induced a decrease in GSH and an increase in ROS levels and iron accumulation
Iron↑,
p‑JNK↑, Curcumin causes mitochondrial damage by promoting phosphorylation of ERK and JNK, resulting in the increased release of ROS and cytochrome c into the cytoplasm, thereby triggering a mitochondrion-dependent pathway of apoptosis
Cyt‑c↑,
ATF6↑, thyroid cancer with curcumin, both activating transcription factor (ATF) 6 and the ER stress marker C/EBP homologous protein (CHOP) were activated by curcumin and Ca2+-ATPase activity was also affected.
CHOP↑,

2822- CUR,    Identification of curcumin derivatives as human glyoxalase I inhibitors: A combination of biological evaluation, molecular docking, 3D-QSAR and molecular dynamics simulation studies
- Analysis, Nor, NA
GLO-I↓, In present study, a series of curcumin derivatives with high inhibitory activity against human GLO I were discovered. Inhibition constant (K(i)) values of compounds 8, 9, 10, 11 and 13 to GLO I are 4.600μM, 2.600μM, 3.200μM, 3.600μM and 3.600μM,

2823- CUR,    Binding of curcumin with glyoxalase I: Molecular docking, molecular dynamics simulations, and kinetics analysis
- Study, Nor, NA
GLO-I↓, recent studies demonstrate that the nature product curcumin is an efficient inhibitor of GLOI, but its binding mechanism towards GLOI is still unclear.

2974- CUR,    Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition, and E-Cadherin Upregulation in Colorectal Cancer
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, CRC, HCT15 - in-vitro, CRC, COLO205 - in-vitro, CRC, SW-620 - in-vivo, NA, NA
TumCMig↓, Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo.
TumCI↓,
TumCG↓,
TumMeta↓,
Sp1/3/4↓, curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells.
HDAC4↓,
FAK↓, Curcumin inhibits focal adhesion kinase (FAK) phosphorylation
CD24↓, Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells
E-cadherin↑, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT.
EMT↓,
TumCP↓,
NF-kB↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
AP-1↝,
STAT3↓, downregulation of CD24 reduces STAT and FAK activity, decreases cell proliferation, metastasis in human tumor
P53?,
β-catenin/ZEB1↓, CUR could activate protein kinase D1 (PKD1) suggesting that suppressing of β-catenin transcriptional activity prevents growth of prostate cancer
NOTCH1↝,
Hif1a↝,
PPARα↝,
Rho↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
MMP2↓,
MMP9↓,

1617- EA,  CUR,    The inhibition of human glutathione S-transferases activity by plant polyphenolic compounds ellagic acid and curcumin
- in-vitro, Nor, NA
Dose∅, ellagic acid and curcumin were shown to inhibit GSTs A1-1, A2-2, M1-1, M2-2 and P1-1with IC50 values ranging from 0.04 to 5 μM
GSTs↓,

1619- EA,  CUR,    Antimutagenic Effect of the Ellagic Acid and Curcumin Combinations
- in-vitro, Nor, NA
eff↑, In both strains, the antimutagenic activity of two combinations (3 μg of EA+3 μg of CRC and 30 μg of EA+30 μg of CRC mixed with 1 μg of AFB1) was significantly higher

649- EGCG,  CUR,  PI,    Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets
- Review, Var, NA
*BioEnh↑, increase EGCG bioavailability is using other natural products such as curcumin and piperine
EGFR↓,
HER2/EBBR2↓,
IGF-1↓,
MAPK↓,
ERK↓, reduction in ERK1/2 phosphorylation
RAS↓,
Raf↓, Raf-1
NF-kB↓, Numerous investigations have proven that EGCG has an inhibitory effect on NF-κB
p‑pRB↓, EGCG were displayed to reduce the phosphorylation of Rb, and as a result, cells were arrested in G1 phase
TumCCA↑, arrested in G1 phase
Glycolysis↓, EGCG has been found to inhibit key enzymes involved in glycolysis, such as hexokinase and pyruvate kinase, thereby disrupting the Warburg effect and inhibiting tumor cell growth
Warburg↓,
HK2↓,
Pyruv↓,

652- EGCG,  VitK2,  CUR,    Case Report of Unexpectedly Long Survival of Patient With Chronic Lymphocytic Leukemia: Why Integrative Methods Matter
- Case Report, CLL, NA
Remission↑, patient has remained asymptomatic for more than 15 years

685- EGCG,  CUR,  SFN,  RES,  GEN  The “Big Five” Phytochemicals Targeting Cancer Stem Cells: Curcumin, EGCG, Sulforaphane, Resveratrol and Genistein
- Analysis, NA, NA
Bcl-2↓,
survivin↓,
XIAP↓,
EMT↓,
Apoptosis↑,
Nanog↓,
cMyc↓,
OCT4↓,
Snail↓,
Slug↓,
Zeb1↓,
TCF↓,

831- GAR,  CUR,    Induction of apoptosis by garcinol and curcumin through cytochrome c release and activation of caspases in human leukemia HL-60 cells
- in-vitro, AML, HL-60
Apoptosis↑,
Casp3↑,
MMP↓, 20 microM caused a rapid loss of mitochondrial transmembrane potential
Cyt‑c↑, release of mitochondrial cytochrome c into cytosol
proCasp9↑,
Bcl-2↓,
BAX↑,
PARP↓, degradation of PARP
DNAdam↑,
DFF45↓, through the digestion of DFF-45

797- GAR,  CUR,    Differential effects of garcinol and curcumin on histone and p53 modifications in tumour cells
- in-vitro, BC, MCF-7 - in-vitro, OS, U2OS - in-vitro, OS, SaOS2
TumCP↓,
H3K18↓, Garcinol treatment resulted in a strong reduction in H3K18 acetylation, which is required for S phase progression.
DNAdam↑,

808- GAR,  CUR,    Synergistic effect of garcinol and curcumin on antiproliferative and apoptotic activity in pancreatic cancer cells
- in-vitro, PC, Bxpc-3 - in-vitro, PC, PANC1
tumCV↓,
Apoptosis↑, combination of garcinol and curcumin was 2 to 10 fold that of the individual agents
Casp3↑, 2-3x
Casp9↑, 2-3x

1998- Myr,  CUR,    Thioredoxin-dependent system. Application of inhibitors
- Review, Var, NA
TrxR↓, myricetin, which like curcumin, can cause irreversible inhibition of TrxR activity
ROS↑, Curcumin-induced alkylation of TrxR can have effects analogous to NADPH oxidase that involve significant increases in ROS production and increased oxidative stress

150- NRF,  CUR,  docx,    Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells
- in-vitro, Pca, C4-2B
p‑Akt↓,
p‑eIF2α↑, phosphorylated
ER Stress↑, ER stress
ATFs↑, ATF4
CHOP↑,
TRIB3↑,

138- QC,  CUR,    Sensitization of androgen refractory prostate cancer cells to anti-androgens through re-expression of epigenetically repressed androgen receptor - Synergistic action of quercetin and curcumin
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
DNMTs↓,

873- QC,  RES,  CUR,  PI,    Combination Effects of Quercetin, Resveratrol and Curcumin on In Vitro Intestinal Absorption
- in-vitro, Nor, NA
*BioEnh↑, Resveratrol received the greatest enhancement in permeability when combined with other agents: quercetin (310%), curcumin (300%), quercetin and curcumin (323%, 350% with piperine)

918- QC,  CUR,  VitC,    Anti- and pro-oxidant effects of oxidized quercetin, curcumin or curcumin-related compounds with thiols or ascorbate as measured by the induction period method
- Analysis, NA, NA
ROS↑, CUR enhances the prooxidant activity of ascorbate(vit C)
ROS↑, Under anaerobic conditions, QUE, with a catechol ring, may be more prooxidant than CUR, with a phenol ring.

156- Ralox,  Tam,  GEN,  CUR,    Modulators of estrogen receptor inhibit proliferation and migration of prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ERβ↑,

103- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- vitro+vivo, BC, 4T1
ROS↑,
MMP↓,
Bcl-2↓,
BAX↑,
Casp9↑,
T-Cell↑, (CD4+CD8+)
TGF-β↓,

871- RES,  CUR,  QC,    The effect of resveratrol, curcumin and quercetin combination on immuno-suppression of tumor microenvironment for breast tumor-bearing mice
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1
T-Cell↑, in tumor microenviroment
Neut↓,
Macrophages↓,
ROS↑, RCQ significantly increased reactive oxygen species
MMP↓, in cancer cells
other↓, alleviate immunosuppression of the tumor microenvironment to enhance the anti-tumor effect.
AntiTum↑, at least nearly 5 times higher than that of a single Res/Cur/Que  = 1:1:0.5
TumVol↓, 35-47% tumor inhibition rate

2306- SIL,  CUR,  RES,  EA,    Identification of Natural Compounds as Inhibitors of Pyruvate Kinase M2 for Cancer Treatment
- in-vitro, BC, MDA-MB-231
PKM2↓, silibinin, curcumin, resveratrol, and ellagic acid as potential inhibitors of PKM2
Dose↝, IC50 values of 0.91 µM, 1.12 µM, 3.07 µM, and 4.20 µM respectively(enzymatic-assay-based screening)
Dose↝, IC50 against MDA-MB231 cells 208uM, 26uM, 306uM, 20um respectively

139- Tomatine,  CUR,    Combination of α-Tomatine and Curcumin Inhibits Growth and Induces Apoptosis in Human Prostate Cancer Cells
- in-vitro, Pca, PC3
NF-kB↓,
Bcl-2↓,
p‑Akt↓,
p‑ERK↓, ERK1/2

2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. Tq + Cur treatment significantly improved these conditions.
*TNF-α↓,
*IL6↓,
*MRP↓,
*GFR↑,
*mt-ATPase↑, antioxidant enzyme levels and mitochondrial ATPases were restored upon treatment,
*p‑Akt↑, Tq + Cur treatment increased the expressions of phosphorylated Akt, Nrf2 and HO-1 proteins while decreasing the levels of cleaved caspase 3 and NFκB in kidney homogenates.
*NRF2↑,
*HO-1↑,
*Casp3↓,
*NF-kB↓,
*RenoP↑, In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury

119- UA,  CUR,  RES,    Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
ROS⇅, ROS↑ only with CUR alone, otherwise ↓
p‑STAT3↓,
Src↓,
AMPK↑,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 231

Results for Effect on Cancer/Diseased Cells:
14-3-3 proteins↓,1,   p‑4E-BP1↓,1,   p‑ACC-α↑,1,   ACOX1↑,1,   AGRN↓,1,   AIF↑,2,   AKR1C2↓,1,   Akt↓,8,   Akt↑,1,   Akt↝,1,   p‑Akt↓,16,   p‑Akt↝,1,   ALAT↑,1,   Albumin↑,1,   ALDH1A1↓,1,   ALDOA↓,1,   ALP↑,1,   AMPK↑,2,   p‑AMPK↑,1,   angioG↓,2,   angioS↑,1,   AntiCan↑,2,   AntiTum↑,1,   AP-1↓,2,   AP-1↝,2,   Apoptosis↑,42,   Apoptosis↝,2,   AR↓,8,   AR↝,1,   ARE/EpRE↑,1,   AST↑,1,   ATF4↑,1,   ATF6↑,1,   ATFs↑,2,   ATG3↑,2,   ATG5↑,1,   ATP↓,1,   ATPase↓,1,   ATR↑,1,   autolysosome↑,1,   AXIN1↓,1,   BACH1↑,1,   Bacteria↑,1,   BAD↑,1,   BAD↝,1,   p‑BAD↓,2,   Bak↑,1,   BAX↑,17,   BAX↝,2,   Bax:Bcl2↑,3,   Bcl-2↓,29,   Bcl-2↝,1,   Bcl-xL↓,4,   Bcl-xL↝,1,   Beclin-1↑,6,   BID↑,1,   BIM↑,1,   BioAv↓,5,   BioAv↑,10,   BMPs↑,1,   BRCA1↑,1,   CAFs/TAFs↓,1,   Casp3↓,1,   Casp3↑,10,   Casp3↝,1,   cl‑Casp3↑,9,   proCasp3↓,1,   Casp8↑,3,   Casp9↑,8,   cl‑Casp9↑,1,   proCasp9↑,1,   Catalase↓,1,   CBP↓,1,   CD133↓,2,   CD24↓,2,   CD25+↓,1,   CD31↓,1,   CD4+↓,1,   CD44↓,2,   CD44↑,1,   CD8+↑,1,   cDC2↓,2,   CDC25↓,2,   CDK1↓,2,   CDK2↓,1,   CDK4↓,1,   CDK4/6↓,1,   CDK6↓,1,   CDX2↓,1,   chemoP↑,2,   ChemoSen↑,10,   ChemoSideEff↓,1,   cholinesterase↓,1,   CHOP↑,6,   circ-PRKCA↓,1,   cJun↓,1,   CK2↓,1,   p‑cMET↓,1,   cMyc↓,8,   COL2A1↓,1,   COL9A3↓,1,   COMP↓,1,   COX1↓,1,   COX2↓,7,   COX2↝,1,   CPT1A↑,1,   CRP↓,1,   CSCs↓,1,   CT-I↓,1,   CTC↓,1,   CXCc↓,2,   CXCL12↓,1,   CXCR4↓,1,   Cyc↝,1,   cycA1↓,1,   CycB↓,2,   cycD1↓,11,   cycD1↝,1,   cycE1↓,1,   cycF↓,1,   CYP11A1↓,1,   CYP17A1↓,1,   CYP19↓,1,   Cyt‑c↑,7,   Cyt‑c↝,1,   DCells↑,1,   DFF45↓,1,   DGAT1↓,1,   DHT↓,1,   DLC1↑,2,   DNA-PK↑,1,   DNAdam↑,6,   mt-DNAdam↑,1,   DNMT1↓,3,   DNMT3A↓,2,   DNMT3A↑,1,   DNMTs↓,2,   Dose?,1,   Dose↑,3,   Dose↝,6,   Dose∅,5,   DR5↑,1,   E-cadherin↓,3,   E-cadherin↑,12,   ECAR↓,1,   ECM/TCF↓,1,   EFEMP↓,1,   eff↓,4,   eff↑,13,   eff↝,1,   EGF↑,1,   EGFR↓,7,   EGFR↝,1,   p‑eIF2α↑,2,   EIF4E↓,1,   Elvol3↓,1,   EMT↓,15,   ENO2↓,1,   EP300↓,1,   EpCAM↓,1,   EPR↑,1,   ER Stress↑,5,   ER(estro)↓,1,   ERCC1↓,1,   ERK↓,2,   ERK↑,1,   p‑ERK↓,5,   p‑ERK↑,4,   ERβ↑,1,   EZH2↓,3,   FAK↓,1,   Fas↑,1,   fascin↓,1,   FASN↓,2,   Fenton↑,1,   Ferritin↓,1,   Ferroptosis↑,2,   FGF↓,1,   Fibronectin↓,3,   FOXD3↑,1,   Foxm1↓,2,   FoxP3+↓,1,   FTH1↑,1,   FTL↑,1,   GADD45A↑,1,   Galectin-9↓,1,   GAPDH↓,1,   Gli1↓,5,   Gli1↝,1,   GLI2↝,1,   GLO-I↓,4,   GlucoseCon↓,3,   GLUT1↓,1,   Glycolysis↓,5,   GM-CSF↓,2,   GP1BB↓,1,   GPx↓,2,   GPx1↓,1,   GPx4↓,3,   GRP78/BiP↓,1,   GRP78/BiP↑,1,   GSH↓,8,   mt-GSH↓,1,   GSH/GSSG↓,1,   GSK‐3β↓,2,   GSK‐3β↝,1,   GSTP1/GSTπ↓,1,   GSTs↓,1,   H19↓,1,   H3K18↓,1,   Half-Life↝,1,   Half-Life∅,1,   HATs↓,1,   HCAR1↓,2,   HDAC↓,2,   HDAC1↓,1,   HDAC3↓,1,   HDAC4↓,1,   HDAC8↓,1,   HER2/EBBR2↓,3,   HH↓,5,   HIF-1↓,1,   Hif1a↓,4,   Hif1a↝,1,   Hippo↑,1,   HK2↓,3,   HO-1↓,1,   HO-1↑,3,   HSD3B↓,1,   HSF1↓,1,   HSP27↑,1,   HSP70/HSPA5↓,1,   HSP70/HSPA5↑,1,   e-HSP70/HSPA5↓,1,   hTERT↓,1,   Id1↓,1,   IFN-γ↓,1,   IFN-γ↑,1,   IGF-1↓,2,   p‑IKKα↓,1,   IL1↓,2,   IL10↓,1,   IL12↓,1,   IL18↓,1,   IL2↓,1,   IL5↓,1,   IL6↓,5,   IL6↝,1,   IL8↓,1,   IR↓,2,   IRF3↓,1,   Iron↑,4,   IronCh↑,1,   IRP1↑,1,   ITGB1↓,1,   ITGB4↓,1,   ITGB6↓,1,   IκB↓,1,   JAK↓,2,   p‑JAK↓,1,   JAK2↓,1,   p‑JAK2↓,1,   p‑JAK3↓,1,   JNK↓,1,   JNK↑,3,   JNK↝,1,   p‑JNK↓,1,   p‑JNK↑,2,   p‑Jun↑,1,   KCNQ1OT1↓,1,   lactateProd↓,3,   LAMA5↓,1,   LAMs↓,1,   LAR↓,1,   LC3‑Ⅱ/LC3‑Ⅰ↑,3,   LC3I↓,1,   LC3II↓,1,   LC3II↑,2,   LC3s↑,1,   LDHA↓,3,   LDHB↓,1,   LGR5↓,2,   lipid-P↓,1,   lipid-P↑,2,   LOX1↓,1,   Macrophages↓,1,   MAOA↓,1,   MAPK↓,3,   MAPK↑,1,   Matr↓,1,   Mcl-1↓,4,   Mcl-1↑,1,   MCT1↓,2,   MCT4↓,1,   MDA↑,3,   MDM2↓,2,   MDR1↓,1,   MDSCs↓,2,   MeCP2↓,1,   MEG3↑,1,   MEK↓,1,   MET↓,1,   miR-130a↓,1,   miR-142-3p↑,1,   miR-143↑,1,   miR-19b↓,1,   miR-205↑,1,   miR-21↓,3,   miR-25-5p↓,1,   miR-27a-3p↓,3,   miR-29b↓,1,   miR-29b↑,1,   miR-301a-3p↓,1,   miR-30a-5p↑,1,   miR-320a↓,1,   miR-330-5p↑,1,   miR-340↑,1,   miR-34a↑,4,   miR-384↑,1,   miR-409-3p↑,1,   miR-497↑,1,   miR-548ah-5p↑,1,   miR-7641↓,1,   MKP5↑,1,   MMP↓,9,   MMP2↓,5,   MMP2↝,1,   MMP9↓,8,   pro‑MMP9↓,1,   MMPs↓,1,   MPT↑,1,   MRGPRF↓,1,   MRP↓,1,   mtDam↑,4,   mTOR↓,7,   mTOR↝,1,   p‑mTOR↓,6,   MUC1↓,1,   Myc↓,1,   MyD88↓,1,   N-cadherin↓,8,   n-MYC↓,1,   NA↓,1,   NA↑,1,   NADPH↓,1,   Nanog↓,3,   NBR2↑,1,   NEDD9↓,2,   Neurog1↑,1,   neuroP↑,1,   Neut↓,1,   NF-kB↓,27,   NF-kB↝,1,   NFE2L2↑,1,   NK cell↑,1,   NKD2↑,2,   NNMT↓,1,   NO↓,1,   NO↑,1,   NOTCH1↓,4,   NOTCH1↝,1,   NQO1↑,1,   NRF2↓,1,   NRF2↑,4,   NRF2↝,1,   OCT4↓,4,   OS↓,1,   OS↑,1,   other↓,1,   other↑,1,   OXPHOS↑,1,   P-gp↓,1,   p16↑,2,   P21↑,11,   P21↝,1,   p27↑,3,   p300↓,1,   p38↓,1,   p‑p38↑,2,   p‑p42↓,1,   p‑p44↓,1,   p50↓,1,   P53?,1,   P53↓,1,   P53↑,7,   P53↝,1,   p‑P53↑,2,   p62↓,5,   p62↑,3,   p65↓,3,   p‑p65↓,1,   p‑p70S6↓,1,   p‑P70S6K↓,1,   p73↑,1,   PAK↓,1,   PAO↑,1,   Paraptosis↑,1,   PARP↓,1,   PARP↑,3,   p‑PARP↑,1,   cl‑PARP↑,7,   PARP1↓,1,   cl‑PARP1↑,1,   PCLAF↓,1,   PCNA↓,2,   PD-1↓,1,   PD-L1↓,2,   PD-L2↓,1,   PDGF↓,1,   p‑PDGF↓,1,   PDK1↓,1,   p‑PDK1↓,1,   PFK1↓,1,   PFKP↓,1,   PGAM1↓,1,   PGC1A↑,1,   PGE2↓,1,   PGK1↓,1,   PGM1↓,1,   pH↑,2,   PI3K↓,2,   PI3K↝,1,   p‑PI3K↓,1,   PI3K/Akt↓,2,   PI3k/Akt/mTOR↓,3,   PI3K/mTOR/ETS2↓,1,   PIAS-3↑,1,   p‑PIK3R1↓,1,   PIR↓,1,   Pirin↓,1,   PKM2↓,6,   circ‑PLEKHM3↑,1,   PPARα↝,1,   PPARγ↑,1,   p‑pRB↓,1,   PRKCG↑,1,   PSA↓,4,   PSA↝,1,   PSMB5↓,1,   PTCH1↓,1,   PTEN↑,4,   PTEN↝,1,   PTP1B↓,1,   PUMA↑,1,   Pyruv↓,1,   QoL↑,1,   RAD51↑,1,   radioP↑,2,   RadioS↑,5,   RadioS∅,1,   Raf↓,2,   RAS↓,2,   REL↑,1,   Remission↑,1,   Rho↓,1,   ROS↓,3,   ROS↑,43,   ROS⇅,1,   ROS↝,1,   RPS6KA1↓,1,   RTK-RAS↓,1,   p‑S6↓,1,   S6K↓,1,   p‑S6K↓,1,   SCD1↓,1,   SDH↑,1,   selectivity↑,4,   SFRP5↑,1,   Shh↓,5,   Slug↓,3,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   SMG1↑,1,   Smo↓,2,   Snail↓,3,   SNCG↓,1,   SOCS-3↑,1,   SOCS1↑,1,   SOD1↓,1,   SOX2↓,2,   SOX9?,1,   Sp1/3/4↓,6,   SPARC↓,1,   Src↓,2,   SRD5A1↑,1,   SREBF2↓,1,   SSAT↑,1,   StAR↓,1,   STAT↓,1,   STAT1↓,2,   p‑STAT1↓,2,   p‑STAT2↓,1,   STAT3↓,11,   p‑STAT3↓,2,   STAT4↓,1,   STAT5↓,1,   survivin↓,4,   T-Cell↑,5,   TAp63α↑,2,   TAZ↓,1,   p‑TAZ↑,1,   TCA↑,1,   TCF↓,3,   testos↓,1,   TET1↑,2,   TFAP2A↓,1,   TfR1/CD71↑,1,   TGF-β↓,6,   TILs↑,1,   TIM-3↓,1,   TLR4↓,3,   TNF-α↝,1,   TOP1↓,1,   TOP1↑,1,   TOP2↓,1,   TOP2↑,2,   toxicity↓,1,   TP53↑,1,   TRAILR↑,1,   TregCell↓,1,   TRIB3↑,1,   TRIF↓,1,   Trop2↓,1,   Trx↓,1,   Trx1↓,3,   Trx2↓,1,   TrxR↓,6,   TrxR1↓,1,   TumAuto↓,1,   TumAuto↑,11,   TumCCA↑,21,   TumCD↑,2,   TumCG↓,12,   TumCI↓,8,   TumCMig↓,13,   TumCP↓,24,   tumCV↓,7,   TumMeta↓,3,   TumVol↓,6,   Twist↓,1,   uPA↓,1,   UPR↑,1,   USF1↑,1,   VEGF↓,7,   VEGF↝,1,   Vim↓,11,   Vim↑,1,   Warburg↓,2,   Wnt↓,5,   Wnt/(β-catenin)↓,2,   xCT↓,1,   XIAP↓,3,   ZBTB10↑,1,   Zeb1↓,2,   ZO-1↑,1,   α-SMA↓,2,   β-catenin/ZEB1↓,11,   β-catenin/ZEB1↝,1,   p‑β-catenin/ZEB1↑,1,   β-TRCP↑,1,   γH2AX↑,2,   p‑γH2AX↑,1,  
Total Targets: 562

Results for Effect on Normal Cells:
12LOX↑,1,   5LO↓,1,   Ach↑,1,   AChE↓,2,   AIF↓,1,   Akt↓,1,   Akt↑,1,   p‑Akt↑,1,   ALAT↓,2,   ALP↓,1,   AntiAg↑,1,   antiOx↓,3,   antiOx↑,9,   AP-1↓,2,   Apoptosis↓,1,   AST↓,2,   ATP↑,1,   mt-ATPase↑,1,   Aβ↓,4,   BBB↑,3,   Bcl-2↑,1,   BioAv↓,3,   BioAv↑,5,   BioAv↝,2,   BioEnh↑,3,   cardioP↑,1,   Casp3↓,3,   Casp9↓,1,   Catalase↑,4,   ChAT↑,1,   CK2↑,1,   cognitive↑,6,   cognitive∅,1,   COL3A1↓,1,   COX2↓,5,   COX2↑,1,   creat↓,1,   Cyt‑c↓,1,   DNAdam↓,1,   Dose↝,1,   Dose∅,1,   eff↑,3,   Ferritin↑,1,   GFR↑,1,   GPx↑,3,   GSH↑,8,   GSK‐3β↓,1,   GSR↓,1,   GSTs↑,1,   H2O2↓,1,   Half-Life↝,1,   HATs↓,1,   HDAC↑,1,   hepatoP↑,3,   HO-1↑,5,   HO-2↓,1,   ICAM-1↓,1,   IL1↓,1,   IL12↓,1,   IL1β↓,5,   IL2↓,1,   IL2↑,1,   IL4↓,2,   IL6↓,4,   IL8↓,1,   INF-γ↓,2,   Inflam↓,14,   iNOS↓,2,   IronCh↑,3,   LDH↓,1,   LDL↓,1,   lipid-P↓,4,   MAOA↓,1,   MCP1↓,2,   MDA↓,6,   memory↑,4,   miR-22↑,1,   MMP2↓,1,   MMP3↓,1,   MMP9↓,1,   MMPs↑,1,   MRP↓,1,   NADPH↑,1,   neuroP↑,6,   NF-kB↓,8,   NLRP3↓,1,   NO↓,4,   NO↑,1,   NRF2↑,8,   OS↑,1,   p300↓,1,   PGE2↓,3,   PI3K↑,1,   RenoP↑,1,   ROS?,1,   ROS↓,18,   SOD↓,1,   SOD↑,6,   Sp1/3/4↓,2,   STAT↓,1,   STAT3↓,1,   TAC↑,1,   tau↓,1,   TGF-β↓,1,   TIMP1↑,1,   TLR2↓,1,   TNF-α↓,6,   toxicity↓,1,   toxicity∅,1,   α-SMA↓,1,  
Total Targets: 110

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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