OLIG2 Cancer Research Results

OLIG2, oligodendrocyte transcription factor 2: Click to Expand ⟱
Source:
Type:

OLIG2 (oligodendrocyte transcription factor 2) is a basic helix-loop-helix transcription factor that regulates neural progenitor and oligodendrocyte lineage development. In gliomas, particularly diffuse gliomas and glioblastoma, OLIG2 is frequently expressed in tumour-propagating cells and can support proliferation, stem-like properties, lineage plasticity and tumour maintenance. OLIG2 also interacts with cell-cycle and DNA-damage-response programs and can suppress p53-dependent growth arrest in some glioma models. Experimental OLIG2 inhibition or depletion can reduce proliferation and tumourigenic capacity and may promote differentiation. The typical cancer-associated direction is therefore generally up or functionally active in OLIG2-positive gliomas, while the desired anticancer modulation is generally down or transcriptional inhibition.



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: OLIG2, oligodendrocyte transcription factor 2
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#:1603  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page