Database Query Results : Curcumin, , TumCCA

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
-may suppress CSC: suppresses self-renewal and pathways (Wnt/Notch/Hedgehog).
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
curcumin can act as a pro-oxidant when blue light is applied
- 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↓
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

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Label	Primary Interpretation	Notes
1	NF-κB signaling	↓ NF-κB activation	↓ inflammatory NF-κB tone	Driver	Suppression of survival and inflammatory transcription	NF-κB is a primary, repeatedly validated curcumin target explaining pleiotropic downstream effects
2	STAT3 signaling	↓ STAT3 phosphorylation / activity	↔ or mild suppression	Driver	Loss of pro-survival and proliferative signaling	STAT3 inhibition contributes to growth arrest, apoptosis sensitization, and reduced cytokine signaling in tumors
3	Reactive oxygen species (ROS)	↑ ROS (dose- & context-dependent)	↓ ROS / buffered	Conditional Driver	Biphasic redox modulation	Curcumin can act as a pro-oxidant in cancer cells with high basal stress while acting antioxidant in normal cells
4	Mitochondrial integrity / intrinsic apoptosis	↓ ΔΨm; ↑ caspase activation	↔ preserved	Driver	Execution of intrinsic apoptosis	Mitochondrial dysfunction and caspase activation occur downstream of NF-κB/STAT3 and ROS effects
5	PI3K → AKT → mTOR axis	↓ AKT / ↓ mTOR	↔ or adaptive suppression	Secondary	Reduced growth and anabolic signaling	AKT/mTOR inhibition contributes to growth suppression and autophagy induction in cancer cells
6	Autophagy	↑ autophagy (protective or pro-death)	↑ adaptive autophagy	Secondary	Stress adaptation vs cell death	Autophagy may be cytoprotective or cooperate with apoptosis depending on context and dose
7	HIF-1α / VEGF hypoxia–angiogenesis axis	↓ HIF-1α; ↓ VEGF	↔ minimal effect	Secondary	Anti-angiogenic pressure	Suppression of hypoxia-driven transcription limits angiogenesis and tumor adaptation
8	Cell cycle regulation	↑ G2/M or G1 arrest	↔ largely spared	Phenotypic	Cytostatic growth control	Cell-cycle arrest reflects upstream signaling and epigenetic effects rather than direct CDK inhibition
9	Migration / invasion (EMT, MMP axis)	↓ migration & invasion	↔	Phenotypic	Anti-metastatic phenotype	Reduced EMT markers and protease activity limit invasive behavior
10	Epigenetic regulation (p300/CBP HAT activity)	↓ histone acetylation	↔ modest	Secondary	Transcriptional reprogramming	Curcumin modulates chromatin via HAT inhibition rather than classic HDAC inhibition

TumCCA, Tumor cell cycle arrest: Click to Expand ⟱

Source:

Type:

Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.

Scientific Papers found: Click to Expand⟱

147-

ATG,

EGCG,

CUR,

Increased chemopreventive effect by combining arctigenin, green tea polyphenol and curcumin in prostate and breast cancer cells

in-vitro,

Pca,

LNCaP

  5–10μM Cur, 1μM Arc and 40μM EGCG

in-vitro,

Pca,

MCF-7

  5–10μM Cur, 1μM Arc and 40μM EGCG

Bax:Bcl2↑, combination treatment significantly increased the ratio of Bax to Bcl-2 proteins, decreased the activation of NFκB, PI3K/Akt and Stat3
NF-kB↓, arctigenin demonstrated the strongest ability to inhibit the activation of both PI3K/Akt and NFκB pathways in both LNCaP and MCF-7 cells.
PI3K/Akt↓,
STAT3↓,
chemoPv↑, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCP↓, combining Arc and EGCG with Cur to enhance chemoprevention in both prostate and breast cancer.
TumCCA↑, EGCG significantly increased the effect of curcumin on cell cycle arrest at G0/G1 phase in MCF-7 cells, and the effect was further enhanced by the addition of arctigenin
TumCMig↓, EGCG and arctigenin alone or in combination with curcumin significantly decreased the number of migrated MCF-7 cells compared to control

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,

10um(cur), 30uM(AKBA)

mouse

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/CCND1↓,
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↓,

4826-

CUR,

The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management

Review,

Var,

*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

4675-

CUR,

Curcumin improves the efficacy of cisplatin by targeting cancer stem-like cells through p21 and cyclin D1-mediated tumour cell inhibition in non-small cell lung cancer cell lines

in-vitro,

NSCLC,

A549

10–40 µM

ChemoSen↑, we showed that curcumin enhanced the sensitivity of the double-positive (CD166+/EpCAM+) CSC subpopulation in non-small cell lung cancer (NSCLC) cell lines (A549 and H2170) to cisplatin-induced apoptosis and inhibition of metastasis.
CSCs↓, Curcumin enhances the sensitivity of the CSC subpopulation of CD166+/EpCAM+ cells to cisplatin-induced apoptosis
EpCAM↓, curcumin enhanced the inhibitory effects of cisplatin on the highly migratory CD166+/EpCAM+ subpopulation
TumCCA↓, combined treatments induced cell cycle arrest, therefore triggering CSC growth inhibition via the intrinsic apoptotic pathway.
VEGF↓, curcumin markedly decreased the metastasis of breast tumour cells to the lung and suppressed the expression of vascular endothelial growth factor (VEGF), matrix metalloproteinase-9 (MMP-9)
MMP9↓,
toxicity↓, Furthermore, curcumin has been found to be safe when administered at ≤10 g/day in humans

4671-

CUR,

Targeting colorectal cancer stem cells using curcumin and curcumin analogues: insights into the mechanism of the therapeutic efficacy

in-vitro,

CRC,

CSCs↓, Intriguingly, curcumin and its analogues have also recently been shown to be effective in lowering tumour recurrence by targeting the CSC population, hence inhibiting tumour growth.
TumCG↓,
ChemoSen↑, curcumin could play a role as chemosensitiser whereby the colorectal CSCs are now sensitised towards the anti-cancer therapy,
Wnt↓, Three major signaling pathways in which curcumin plays a pivotal role in CSC self-renewal behavior are the Wnt/β-catenin, Sonic Hedgehog (SHH), and Notch pathways
β-catenin/ZEB1↓,
Shh↓,
NOTCH↓,
DNMT1↓, Figure 1
STAT3↓,
NF-kB↓,
EGFR↓,
IGFR↓,
TumCCA↓,
cl‑PARP↑,
BAX↑,
ECM/TCF↓,

4652-

CUR,

Anticancer effect of curcumin on breast cancer and stem cells

Review,

BC,

TumCP↓, inhibiting cancer cell proliferation and metastasis and by inducing cell cycle arrest and apoptosis.
TumMeta↓,
TumCCA↑,
Apoptosis↑,
CSCs↓, curcumin inhibits the proliferation of breast cancer stem cells (BCSC), an important factor that influences cancer recurrence.
NF-kB↓, curcumin exhibited a potent antiproliferation effect by inhibiting the binding activity of NF-KB
Telomerase↓, Curcumin inhibited telomerase activity in human leukemia cells [21,22] and brain tumor cells [23] in a dose-dependent and time-dependent manner.
Cyt‑c↑, curcumin releases cytochrome C and upregulates caspase-9 and caspase-3 expression
Casp9↑,
Casp3↑,
E-cadherin↑, Curcumin inhibits the migratory ability of BSCS by amplifying the E-cadherin/β-catenin negative feedback loop.

2654-

CUR,

Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence

Review,

Var,

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

455-

CUR,

Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin

in-vitro,

GC,

SGC-7901

10, 20, 40 and 80 µM, 48 h

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

50 μM, 24, 48 and 96 h

miR-34a↑,
TumCP↓,
TumCMig↓,
TumCI↓,
TumCCA↑, inhibited cell cycle progression in G0/G1-S phase
Bcl-2↓,
CDK4/6↓, CDK4
cycD1/CCND1↓,

459-

CUR,

Curcumin inhibits cell proliferation and motility via suppression of TROP2 in bladder cancer cells

in-vitro,

Bladder,

T24/HTB-9

10, 15, 20 and 25 µM, 48 and 72 h

in-vitro,

Bladder,

RT4

Trop2↓,
Apoptosis↑,
cycE1↓,
p27↑,
TumCCA↑, curcumin induced G2/M cell cycle arrest

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

15 and 30 μM, 24, 48 and 72 h; 100 mg/kg/day, 14 days

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↑,

437-

CUR,

Anti-cancer activity of amorphous curcumin preparation in patient-derived colorectal cancer organoids

vitro+vivo,

CRC,

TCO1

0.6, 2, 6 and 20 µg/mL, 72 h; 20 mg/day, 21 days

vitro+vivo,

CRC,

TCO2

cycD1/CCND1↓,
cMyc↓,
p‑ERK↓,
CD44↓,
CD133↓,
LGR5↓,
TumCCA↑, proportion of cells in the G0/G1 phase in CRC organoids significantly increased at 24 h
TumVol↓,
CSCs↓, Expressions of CSC markers, CD44, LGR5, and CD133, were declined in the AC-treated CRC organoids.

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

 15uM

vitro+vivo,

MG,

T98G

 31uM
31 uM

HH↓, Both mRNA and protein levels of SHH/GLI1 signaling (Shh, Smo, GLI1) were downregulated in a dose‐ and time‐dependent manner
Shh↓, inhibition of SHH/GLI1 signaling by curcumin may act as a novel mechanism of the apoptosis.
Gli1↓,
cycD1/CCND1↓,
Bcl-2↓,
FOXM1↓,
Bax:Bcl2↑, The Bax/Bcl‐2 ratio (Figure 6D) also gradually increased.
TumCP↓, Curcumin suppressed cell proliferation, colony formation, migration, and induced apoptosis which was mediated partly through the mitochondrial pathway after an increase in the ratio of Bax to Bcl2.
TumCMig↓,
Apoptosis↑,
TumVol↑, Intraperitoneal injection of curcumin in vivo reduced tumor volume,
TumCCA↑, Curcumin Inhibited Proliferation of Human Glioma Cells and induced G2/M Arrest
Casp3↑, level of caspase‐3 increases significantly after curcumin treatment.
OS↑, Curcumin Inhibited GBM Growth in Vivo through SHH/GLI1 Signaling and Prolonged the Survival Period

440-

CUR,

Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells

vitro+vivo,

CRC,

SW480

10, 20, 30, 40, 50 and 60 µM, 24 h; 100 mg/kg/day, 3 weeks

vitro+vivo,

CRC,

HT-29

13.69 μM

NNMT↓,
p‑STAT3↓,
TumCP↓,
TumCCA↑, G2/M phase cell cycle arrest
ROS↑,

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

0-40uM

Apoptosis↑,
TumCP↓,
TumCCA↑, block of G0/G1 phase
TET1↑,
NKD2↑,
Wnt↓,
EMT↓,
Vim↑,
E-cadherin↓,
β-catenin/ZEB1↓,
TCF↓, TCF4
AXIN1↓, Axin

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

15, 20 and 25 μM, 48 h

Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,

452-

CUR,

Curcumin downregulates the PI3K-AKT-mTOR pathway and inhibits growth and progression in head and neck cancer cells

vitro+vivo,

HNSCC,

SCC9

0, 25, 10, 5, 2.5, 1.25 and 0.75 μM, 24 and 48 h

41uM

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

10,- 100 µM, 24, 48 and 72 h; 50 mg/kg, 6weeks

Bcl-2↓,
survivin↓,
BAX↑,
TumCCA↑, Gemini-Cur compound induced G2/M cell cycle arrest

1409-

CUR,

Curcumin analog WZ26 induces ROS and cell death via inhibition of STAT3 in cholangiocarcinoma

in-vivo,

CCA,

Walker256

mouse

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

1411-

CUR,

Cisplatin,

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Review,

Var,

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↑,

1505-

CUR,

Epigenetic targets of bioactive dietary components for cancer prevention and therapy

Review,

NA,

25 μM @24hr

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

474-

CUR,

Modification of radiosensitivity by Curcumin in human pancreatic cancer cell lines

in-vitro,

PC,

PANC1

6, 10 and 12 µM, 24 h

in-vitro,

PC,

MIA PaCa-2

TumCD↑,
Apoptosis↑,
DNAdam↑,
γH2AX↑, yH2AX-MFI
TumCCA↑, radiation-sensitive G2/M-phase

477-

CUR,

Curcumin induces G2/M arrest and triggers autophagy, ROS generation and cell senescence in cervical cancer cells

in-vitro,

Cerv,

SiHa

5, 15, 30 and 50 µM, 6, 12, 24 and 48 h

TumCP↓,
TumCCA↑, Inducing G2/M cell cycle arrest
Apoptosis↑,
TumAuto↑,
CycB/CCNB1↓, cyclins B1
CDC25↓,
ROS↑,
p62↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,
cl‑Casp3↑,
cl‑PARP↑,
P53↑,
P21↑,

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

10, 25, 50 and 100 µM, 16 and 24 h

TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, S-phase cell cycle arrest
Bcl-2↓,
BAX↑,
cl‑Casp3↑,

480-

CUR,

Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells

in-vitro,

GBM,

SNB19

10, 15, 20 and 25 µM, 48 and 72 h

TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, G2/M phase
NEDD9↓,
NOTCH1↓,
p‑Akt↓,

132-

CUR,

Targeting multiple pro-apoptotic signaling pathways with curcumin in prostate cancer cells

in-vitro,

Pca,

PC3

TumCCA↑, inducing a chronic ER stress mediated cell death and activation of cell cycle arrest, UPR, autophagy and oxidative stress responses.
ROS↑, correlating with the upregulation of reactive oxygen species
TumAuto↑,
UPR↑, The upregulation of eIF2α in curcumin-treated cells, suggests activation of the UPR-associated PERK pathway
ER Stress↑,
Casp3↑, Chronic ER stress induction was concomitant with the upregulation of pro-apoptotic markers (caspases 3,9,12) and Poly (ADP-ribose) polymerase.
Casp9↑,
Casp12↑,
PARP↑,
other↝, Curcumin-treated PC3 cells expressed 146 upregulated and 184 downregulated proteins when compared with control PC3 cells (treated with DMSO).
GRP78/BiP↑, GRP78 and the PDI family were upregulated by 1.69 and ≥1.25-fold respectively
PDI↑,
eIF2α↑, other upregulated proteins related to ER stress figure eukaryotic translation initiation factor 2A (EIF2A), with a significant fold change of 1.25,
other↝, downregulated antioxidant markers such as peroxiredoxin 6 (PRDX6) and protein DJ-1 (PARK7) with significant fold changes of –1.39 and –1.51, respectively

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↓, Notch 1 signaling was down regulated in Notch 1 siRNA or Notch 1 plasmid transfected 145 cells after curcumin treatment.
cycD1/CCND1↓, s Cyclin D1 and CDK2 expressions were inhibited.
CDK2↓,
P21↑,
p27↑,
P53↑, apoptosis related protein p53 expression was increased, and apoptosis suppressor Bcl-2 was inhibited in DU-145 after curcumin treatment
Bcl-2↓,
Casp3↑, Caspase-3 and Caspase-9 were activated by curcumin
Casp9↑,
TumCCA↑, Curcumin induced G0/G1 arrest in DU-145 cells,
TumCP↓, Curcumin inhibited proliferation and induced apoptosis in DU-145 cells
Apoptosis↑,

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↑, WZ35 Increased Reactive Oxygen Species (ROS) Accumulation in RM-1 Cells
tumCV↓, Our results showed that WZ35 treatment induced loss of cell viability, cell apoptosis, and G2/M cycle arrest in both RM-1 and DU145 cells, coupled with ROS overproduction, intracellular calcium surge, and activation of mitochondrial apoptosis
Apoptosis↑,
TumCCA↑,
Ca+2↑,
eff↓, ROS also mediated cell cycle arrest in G2/M phase evidenced by the fact that pretreatment with NAC significantly decreased cell accumulation in G2/M phase and CDC2/cyclin B1 protein level in WZ35-treated cells
ER Stress↑, Thus, ER stress may be involved in the anti-prostate cancer effects of WZ35

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

 2.2 μM

 for WZ35 analog. For Curcumin it is 20.9μM

in-vitro,

Pca,

DU145

ROS↑, WZ35 treatment for 30 min significantly induced reactive oxygen species (ROS) production in PC-3 cells.
Bcl-2↓,
PARP↑,
cDC2↓, decreased expression of CDC2, cyclinB1, and MDM2
CycB/CCNB1↓,
MDM2↓,
eff↓, Co-treatment with the ROS scavenger NAC completely abrogated the induction of WZ35 on cell apoptosis,
eIF2α↑, WZ35 treatment also induced a constant increase in the level of phosphorylated eIF2α 3 to 12 h after WZ35 treatment
ATF4↑, ATF4 expression also increased in a similar manner with p-eIF2α
CHOP↑, CHOP protein expression apparently increased 9-24 h after WZ35 treatment and peaked at 12 h
ER Stress↑, results suggest that WZ35 can induce ER stress in prostate cancer cells
TumCCA↑, WZ35 induced cell cycle arrest in G2/M phase in PC-3 cells

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↑, The protein expressions of p21 were significantly increased by the co-treatment of EGCG and curcumin, whereas it was not changed by the treatment with each individual compound.
TumCCA↑, treatments of EGCG and curcumin arrested both S and G2/M phases of PC3 cells.
TumCP↓, EGCG inhibited PC3 cell proliferation to 11.2 and 24.3% at 50 and 100 μM, respectively.
BioAv↓, While curcumin has versatile anticancer properties, its poor absorption and low bioavailability are the challenges for its developmentas chemopreventive agent (33). The low bioavailability of EGCG is also confirmed i

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↓, significantly regulated top canonical pathways highlighted that Transforming growth factor beta (TGF-β), Wingless-related integration site (Wnt), Phosphoinositide 3-kinase/Protein Kinase B/ mammalian target of rapamycin (PIK3/AKT(PKB)/mTOR)
Wnt↓,
PI3k/Akt/mTOR↓,
NF-kB↓, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling were primarily inhibited
PTEN↑,
Apoptosis↑,
TumCCA↑, Phosphatase and tensin homolog (PTEN) dependent cell cycle arrest and apoptosis pathways were elevated with curcumin treatment.

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↓, via Inhibition of NF-κB and AP-1 Pathway in vitro
AP-1↓,
TumCG↓, Curcumin could effectively suppress the in vitro growth of PC-3 cells.
TumCCA↑, Curcumin treatment significantly arrested PC-3 cells in the G 2/M phase

649-

EGCG,

CUR,

PI,

Targeting Cancer Hallmarks with Epigallocatechin Gallate (EGCG): Mechanistic Basis and Therapeutic Targets

Review,

Var,

*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↓,

4904-

Sal,

CUR,

Co-delivery of Salinomycin and Curcumin for Cancer Stem Cell Treatment by Inhibition of Cell Proliferation, Cell Cycle Arrest, and Epithelial–Mesenchymal Transition

CSCs↓, We determined CD44-targeting co-delivery nanoparticles are highly efficacious against BCSCs by inducing G1 cell cycle arrest and limiting epithelial–mesenchymal transition.
TumCCA↑,
EMT↓,
other↝, anti-cancer mechanism of salinomycin is associated with dysregulation of metal ions
TumAuto↑, activation of autophagy-mediated cell death, and inhibition of stem cell maintenance
Iron↑, recent study found that salinomycin and its derivative, ironomycin, exhibited a potent and selective activity against breast cancer stem cells (BCSCs) by accumulating and sequestering iron to induce ferroptosis,
Ferroptosis↑,
BioAv↓, challenging to efficiently deliver salinomycin (Sal) to tumor sites due to its hydrophobicity, unfavorable pharmacokinetic profile, and cytotoxicity during systemic drug administration
ROS↑, Our previous studies showed that conjugation of salinomycin with gold nanoparticles can efficiently induce ferroptotic cell death of BCSCs by increasing the generation of ROS, mitochondrial dysfunction, and lipid oxidation with higher iron accumulati
lipid-P↑,
GPx4↓, and GPX-4 inactivation
eff↑, Salinomycin and curcumin were loaded onto poly(lactic-co-glycolic acid) (PLGA) polymeric nanoparticles via double emulsion method to form nanoparticles . salinomycin and curcumin showed improved therapeutic efficiency against BCSCs

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 34

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↑, 1,
Total Targets: 163

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, ROS↓, 2,

Immune & Inflammatory Signaling ⓘ

Inflam↑, 1, NF-kB↓, 1,

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,
Total Targets: 5

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest

34 Curcumin
3 EGCG (Epigallocatechin Gallate)
2 5-fluorouracil
1 Arctigenin
1 Boswellia (frankincense)
1 Chemotherapy
1 Cisplatin
1 Piperine
1 salinomycin

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:322  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : Curcumin, , TumCCA

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

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