condition found tbRes List
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↓
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


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⟱
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↓,

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↑,

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

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↑,

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↑,

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

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↓,

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

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↓,

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

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

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

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↓,

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↑,

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

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↑,

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

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↓,

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↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Results for Effect on Cancer/Diseased Cells:
Akt↓,2,   p‑Akt↓,3,   Apoptosis↑,12,   AXIN1↓,1,   Bacteria↑,1,   BAD↑,1,   p‑BAD↓,1,   BAX↑,3,   Bcl-2↓,5,   Beclin-1↑,1,   BioAv↑,1,   Casp3↑,1,   cl‑Casp3↑,3,   proCasp3↓,1,   Catalase↓,1,   CD133↓,1,   CD44↓,1,   CDC25↓,1,   CDK4↓,1,   CDK4/6↓,1,   CDK6↓,1,   ChemoSen↑,2,   cMyc↓,2,   CycB↓,1,   cycD1↓,3,   cycE1↓,1,   DNAdam↑,1,   DNMTs↓,1,   E-cadherin↓,1,   E-cadherin↑,1,   eff↓,1,   EGF↑,1,   EGFR↓,2,   EIF4E↓,1,   EMT↓,2,   ER Stress↑,1,   ERK↓,1,   p‑ERK↓,1,   Foxm1↓,1,   Gli1↓,1,   GLO-I↓,1,   Glycolysis↓,1,   GPx1↓,1,   GPx4↓,1,   HATs↓,1,   HDAC↓,1,   HDAC1↓,1,   HDAC3↓,1,   HDAC8↓,1,   HER2/EBBR2↓,1,   HK2↓,1,   HSP27↑,1,   IGF-1↓,1,   JNK↑,1,   LC3‑Ⅱ/LC3‑Ⅰ↑,1,   LGR5↓,1,   MAPK↓,1,   miR-27a-3p↓,2,   miR-34a↑,3,   MMP↓,1,   p‑mTOR↓,1,   NADPH↓,1,   NEDD9↓,1,   NF-kB↓,2,   NKD2↑,1,   NNMT↓,1,   NOTCH1↓,1,   P21↑,1,   p27↑,1,   p300↓,1,   P53↑,1,   p62↑,2,   cl‑PARP↑,2,   PARP1↓,1,   p‑PI3K↓,1,   PI3k/Akt/mTOR↓,2,   p‑pRB↓,1,   PRKCG↑,1,   Pyruv↓,1,   Raf↓,1,   RAS↓,1,   ROS↑,6,   RPS6KA1↓,1,   Shh↓,1,   SOD1↓,1,   STAT3↓,2,   p‑STAT3↓,1,   survivin↓,1,   TCF↓,1,   TET1↑,1,   Trop2↓,1,   TumAuto↑,2,   TumCCA↑,21,   TumCD↑,1,   TumCG↓,2,   TumCI↓,1,   TumCMig↓,4,   TumCP↓,7,   TumVol↓,1,   UPR↑,1,   Vim↓,1,   Vim↑,1,   Warburg↓,1,   Wnt↓,2,   β-catenin/ZEB1↓,2,   γH2AX↑,1,  
Total Targets: 106

Results for Effect on Normal Cells:
BioEnh↑,1,   NF-kB↓,1,   ROS↓,1,  
Total Targets: 3

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
21 Curcumin
2 5-fluorouracil
1 Boswellia (frankincense)
1 Chemotherapy
1 Cisplatin
1 EGCG (Epigallocatechin Gallate)
1 Piperine
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:322  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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