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.


GC, Gastric Adenocarcinoma: Click to Expand ⟱
Stomach/Gastric Cancer

Scientific Papers found: Click to Expand⟱
5541- BBM,    Berbamine Suppresses the Growth of Gastric Cancer Cells by Inactivating the BRD4/c-MYC Signaling Pathway
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓, TumCCA↑, Apoptosis↑, BRD4↓, selectivity↑, TumCG↓, cMyc↓,
1607- EA,    Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions
- Review, GC, NA
STAT3↓, TumCP↓, Apoptosis↑, NF-kB↓, EMT↓, RadioS↑, antiOx↑, COX1↓, COX2↓, cMyc↓, Snail↓, Twist↓, MMP2↓, P90RSK↓, CDK8↓, PI3K↓, Akt↓, TumCCA↑, Casp8↑, PCNA↓, TGF-β↓, Shh↓, NOTCH↓, IL6↓, ALAT↓, ALP↓, AST↓, VEGF↓, P21↑, *toxicity∅, *Inflam↓, *cardioP↑, *neuroP↑, *hepatoP↑, ROS↑, *NRF2↓, *GSH↑,
1013- Lyco,    Lycopene induces apoptosis by inhibiting nuclear translocation of β-catenin in gastric cancer cells
- in-vitro, GC, AGS
Apoptosis↑, DNAdam↑, Bax:Bcl2↑, ROS↓, β-catenin/ZEB1↓, p‑GSK‐3β↓, APC↑, β-TRCP↑, cMyc↓, cycD1/CCND1↓,
4793- Lyco,    Lycopene treatment inhibits activation of Jak1/Stat3 and Wnt/β-catenin signaling and attenuates hyperproliferation in gastric epithelial cells
- in-vitro, GC, AGS
antiOx↑, AntiCan↑, ROS↓, JAK1↓, STAT3↓, Wnt↓, β-catenin/ZEB1↓, cMyc↓, cycE/CCNE↓, TumCP↓, Risk↓,
2234- SK,    Shikonin Suppresses Cell Tumorigenesis in Gastric Cancer Associated with the Inhibition of c-Myc and Yap-1
- in-vitro, GC, NA
TumCP↓, TumCI↓, TumCMig↓, cMyc↓, YAP/TEAD↓,

Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

antiOx↑, 2,   ROS↓, 2,   ROS↑, 1,  

Core Metabolism/Glycolysis

ALAT↓, 1,   cMyc↓, 5,  

Cell Death

Akt↓, 1,   Apoptosis↑, 3,   Bax:Bcl2↑, 1,   Casp8↑, 1,   YAP/TEAD↓, 1,   β-TRCP↑, 1,  

Transcription & Epigenetics

BRD4↓, 1,  

DNA Damage & Repair

DNAdam↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence

BRD4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State

CDK8↓, 1,   EMT↓, 1,   p‑GSK‐3β↓, 1,   NOTCH↓, 1,   P90RSK↓, 1,   PI3K↓, 1,   Shh↓, 1,   STAT3↓, 2,   TumCG↓, 1,   Wnt↓, 1,  

Migration

APC↑, 1,   MMP2↓, 1,   Snail↓, 1,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   Twist↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature

VEGF↓, 1,  

Immune & Inflammatory Signaling

COX1↓, 1,   COX2↓, 1,   IL6↓, 1,   JAK1↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance

RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   IL6↓, 1,  

Functional Outcomes

AntiCan↑, 1,   Risk↓, 1,  
Total Targets: 52

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

GSH↑, 1,   NRF2↓, 1,  

Immune & Inflammatory Signaling

Inflam↓, 1,  

Functional Outcomes

cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   toxicity∅, 1,  
Total Targets: 7

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene
2 Lycopene
1 Berbamine
1 Ellagic acid
1 Shikonin
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:28  Cells:%  prod#:%  Target#:35  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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