cMyc Cancer Research Results

cMyc, cellular-MYC oncogene: Click to Expand ⟱
Source:
Type: oncogene
The MYC proto-oncogenes are among the most commonly activated proteins in human cancer. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. The c-Myc oncogene is a ‘master regulator’ of both cellular growth and metabolism in transformed cells.
-C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A

Inhibitors (downregulate):
Curcumin
Resveratrol: downregulate c-Myc expression.
Epigallocatechin Gallate (EGCG)
Quercetin
Berberine: decrease c-Myc expression and repress its transcriptional activity.
Melanoma, Melanoma Skin Cancer: Click to Expand ⟱
Melanoma is a rare form of skin cancer. It is more likely to invade nearby tissues and spread to other parts of the body than other types of skin cancer.
Scientific Papers found: Click to Expand⟱
6691- DFC,    Diclofenac impairs the proliferation and glucose metabolism of triple-negative breast cancer cells by targeting the c-Myc pathway
- in-vitro, Melanoma, NA - in-vitro, BC, MDA-MB-231 - in-vitro, BC, HCC1937 - in-vitro, BC, MCF7
Glycolysis↓, Apoptosis↑, cMyc↓, GLUT1↓, TumCP↓, HK2↓, TumCP↓,
7060- GamB,    New targets for the antitumor activity of gambogic acid in hematologic malignancies
- Review, Melanoma, RPMI-8226
AntiCan↑, TumCP↓, Apoptosis↑, SRC3↓, DIDO1/DIO-1↑, KCNH2/hERG↓, ROS↑, Bcl-2↓, P53↑, cMyc↓, VEGF↓, Casp3↑, cl‑PARP1↑, eff↓,
1020- UA,    Root Bark of Morus alba L. and Its Bioactive Ingredient, Ursolic Acid, Suppress the Proliferation of Multiple Myeloma Cells by Inhibiting Wnt/β-Catenin Pathway
- in-vitro, Melanoma, RPMI-8226
β-catenin/ZEB1↓, TCF↓, cMyc↓, cycD1/CCND1↓, TumCP↓, TumCCA↑, Apoptosis↑, cl‑Casp3↑, cl‑PARP↑, Casp7↑,

Showing Research Papers: 1 to 3 of 3

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

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

DIDO1/DIO-1↑, 1,   KCNH2/hERG↓, 1,   SRC3↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 3,   Glycolysis↓, 1,   HK2↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 3,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp7↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   cl‑PARP↑, 1,   cl‑PARP1↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

TCF↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 4,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene
1 Diclofenac
1 Gambogic Acid
1 Ursolic acid
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:39  Cells:%  prod#:%  Target#:35  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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