MYCN Cancer Research Results

MYCN, MYCN proto-oncogene: Click to Expand ⟱
Source:
Type:

MYCN (MYCN proto-oncogene; N-Myc) is a member of the MYC family of basic helix-loop-helix transcription factors that regulates genes involved in cell growth, proliferation, metabolism, ribosome biogenesis, differentiation and apoptosis. MYCN amplification or overexpression is strongly oncogenic and is particularly important in neuroblastoma, where amplification is associated with aggressive disease, increased tumour progression and poor prognosis. Increased MYCN activity promotes proliferative and metabolic programs, inhibits neuronal differentiation and can enhance glycolysis, angiogenesis, stemness and metastatic behaviour. Experimental MYCN suppression can reduce proliferation, promote differentiation and inhibit tumour growth. The typical cancer-associated direction is therefore up, while the desired anticancer modulation is down, transcriptional suppression or destabilization of the MYCN protein. MYCN is separate from MYC (c-Myc) and MYCL, which are related but distinct MYC-family oncogenes.



Scientific Papers found: Click to Expand⟱
7171- CHA,    Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201
- vitro+vivo, GBM, DIPG
TumCG↓, High-throughput small-molecule screening identified an epigenetic compound chaetocin as a potent blocker of DIPG cell growth
TumCP↓, Chaetocin treatment selectively decreased proliferation and increased apoptosis of DIPG cells and significantly extended survival in DIPG xenograft models, while restoring H3K27me3 levels
Apoptosis↓,
OS↑,
H3K9↓, he loss of H3K9 methyltransferase SUV39H1 inhibited DIPG cell growth.
SUV39H↓, SUV39H1 and H3K9me3 Levels Are Downregulated by Chaetocin Treatment
eff↑, Consistently, a combination of chaetocin treatment with a DRD2 antagonist ONC201 synergistically increased the antitumor efficacy.
CSCs↓, SUV39H1 Inhibition Decreases Stemness and Oncogenic Signaling
SOX9↓, chaetocin treatment and SUV39H1 depletion led to decreased expression of genes associated with stemness (eg, SOX9, MYCN, OLIG2, AURKB), growth factor signaling (eg, HGF, FGF21), receptor-tyrosine kinases signaling (eg, EGFR, FGFR, and PDGFR), and WNT
HGF/c-Met↓,
FGF21↓,
EGFR↓,
PDGFR-BB↓,
Wnt↓,
MYCN↑,
OLIG2↓,
AURKB↓,
HO-1↑, genes associated with the NRF2 stress pathway, oxidative stress-related genes (eg, HMOX1, ARK1C1), cell cycle inhibition (eg, CDKN1A, CDKN2B, CDKN2D), and neuronal signaling activity (eg, DRD2, NRG1, NRXN1) were upregulated
P21↑,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

AURKB↓, 1,   H3K9↓, 1,   MYCN↑, 1,   OLIG2↓, 1,   SUV39H↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

FGF21↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   HGF/c-Met↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

SOX9↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↑, 1,  

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

CSCs↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   PDGFR-BB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

OS↑, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: MYCN, MYCN proto-oncogene
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:%  Cells:%  prod#:%  Target#:1602  State#:%  Dir#:2
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