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.


Lung, Lung Cancer: Click to Expand ⟱
Lung CSC (Cancer Stem Cells) markers (CD133, CD44, ALDHA1, Nanog and Oct4)

Scientific Papers found: Click to Expand⟱
5695- BRU,    Brusatol enhances the efficacy of chemotherapy by inhibiting the Nrf2-mediated defense mechanism
- in-vitro, Lung, A549
NRF2↓, ChemoSen↑, Apoptosis↑, TumCP↓, TumCG↓, MRP1↓, GSH↓, cMyc↓,
2940- PL,    Piperlongumine Induces Reactive Oxygen Species (ROS)-dependent Downregulation of Specificity Protein Transcription Factors
- in-vitro, PC, PANC1 - in-vitro, Lung, A549 - in-vitro, Kidney, 786-O - in-vitro, BC, SkBr3
ROS↑, TumCP↓, Apoptosis↑, eff↓, Sp1/3/4↓, cycD1/CCND1↓, survivin↓, cMyc↓, EGFR↓, cMET↓,
4666- RES,    Structural modification of resveratrol analogue exhibits anticancer activity against lung cancer stem cells via suppression of Akt signaling pathway
- in-vitro, Lung, H23 - in-vitro, Lung, H292 - in-vitro, Lung, A549
CSCs↓, eff↑, Akt↓, GSK‐3β↑, SOX2↓, cMyc↓, TumCCA↑, ROS↑, Apoptosis↑,

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:


Redox & Oxidative Stress

GSH↓, 1,   NRF2↓, 1,   ROS↑, 2,  

Core Metabolism/Glycolysis

cMyc↓, 3,  

Cell Death

Akt↓, 1,   Apoptosis↑, 3,   survivin↓, 1,  

Kinase & Signal Transduction

Sp1/3/4↓, 1,  

Cell Cycle & Senescence

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State

cMET↓, 1,   CSCs↓, 1,   GSK‐3β↑, 1,   SOX2↓, 1,   TumCG↓, 1,  

Migration

TumCP↓, 2,  

Angiogenesis & Vasculature

EGFR↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,   eff↓, 1,   eff↑, 1,   MRP1↓, 1,  

Clinical Biomarkers

EGFR↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene
1 brusatol
1 Piperlongumine
1 Resveratrol
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:15  Cells:%  prod#:%  Target#:35  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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