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


DNMT3A, DNA (cytosine-5-)-methyltransferase 3 alpha: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
DNA (cytosine-5-)-methyltransferase 3 alpha, commonly referred to as DNMT3A, is an enzyme that plays a crucial role in the process of DNA methylation, which is an important mechanism for regulating gene expression and maintaining genomic stability.
The expression levels of DNMT3A and the presence of mutations can serve as prognostic markers in certain cancers.
In some cancers, DNMT3A is overexpressed, leading to increased DNA methylation of tumor suppressor genes.
Scientific Papers found: Click to Expand⟱
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↑,

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↓,

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


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Results for Effect on Cancer/Diseased Cells:
BRCA1↑,1,   CDX2↓,1,   cMyc↓,1,   cycD1↓,1,   DNMT1↓,2,   DNMT3A↓,2,   DNMT3A↑,1,   E-cadherin↑,2,   EMT↓,2,   Fibronectin↓,1,   miR-29b↓,1,   miR-29b↑,1,   N-cadherin↓,1,   SFRP5↑,1,   Snail↓,1,   SNCG↓,1,   TET1↑,1,   Twist↓,1,   Vim↓,2,   Wnt↓,1,   Wnt/(β-catenin)↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 22

Results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: DNMT3A, DNA (cytosine-5-)-methyltransferase 3 alpha
3 Curcumin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:86  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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