AURKB Cancer Research Results

AURKB, Aurora kinase B: Click to Expand ⟱
Source:
Type:

AURKB (Aurora kinase B) is a serine/threonine kinase and core component of the chromosomal passenger complex, together with INCENP, survivin (BIRC5) and borealin (CDCA8). AURKB regulates chromosome condensation and segregation, correction of kinetochore–microtubule attachment errors, the spindle assembly checkpoint and cytokinesis. AURKB is frequently overexpressed or hyperactive in cancer and can promote chromosomal instability, aneuploidy, rapid proliferation, tumour progression and treatment resistance. Experimental AURKB inhibition causes defective chromosome segregation and cytokinesis, polyploidy, mitotic catastrophe, cell-cycle arrest and apoptosis or senescence. The typical cancer-associated direction is therefore up, while the desired anticancer modulation is generally down or kinase inhibition. AURKB is separate from AURKA and AURKC because the three Aurora kinases have distinct cellular functions and cancer associations.



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: AURKB, Aurora kinase B
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#:1604  State#:%  Dir#:1
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