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BIOMARKER:

AURKB overexpression

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Other names: AURKB, Aurora Kinase B, AIM-1, ARK2, STK5, Protein Phosphatase 1, Regulatory Subunit 48, Serine/Threonine-Protein Kinase Aurora-B, Serine/Threonine-Protein Kinase 12, Serine/Threonine-Protein Kinase 5, Aurora/IPL1-Related Kinase 2, Serine/Threonine Kinase 12, Aurora-Related Kinase 2, Aurora-B, Aurora-1, PPP1R48, ARK-2, STK-1, STK12, AIK2, AIM1, AurB, IPL1, Aurora- And Ipl1-Like Midbody-Associated Protein 1, Aurora- And IPL1-Like Midbody-Associated Protein 1, Aurora Kinase B-Sv1, Aurora Kinase B-
Entrez ID:
2ms
Aurora kinase B expression shields HNSCC from PI3K inhibition-induced apoptosis through downstream mediators AKT and PDK1 (AACR 2022)
To use a pharmacologic approach, we combined the pan-Aurora kinase inhibitor danusertib (0-2µM) with PI3K/mTOR inhibitor omipalisib (0-200nM) in 56 HNSCC cell lines for 72h and observed a substantial decrease in cell viability in >80% of NOTCH1WT and >90% of NOTCH1MUT HNSCC lines...Mice bearing NOTCH1MUT xenografts showed complete tumor regression when treated with a combination of pan-PI3K inhibitor Copanlisib and Aurora inhibitor Alisertib as compared to control groups...We identified AURKB as a central player governing the sensitivity to PI3K inhibitor-induced apoptosis in the context of NOTCH1 mutation status in HNSCC through its effects on AKT and PDK1. These novel findings may lead to the development of more robust therapeutic approach for NOTCH1 mutant squamous carcinoma as well as patients who develop acquired resistance to targeted therapies.
PARP Biomarker
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NOTCH1 (Notch 1) • AURKA (Aurora kinase A) • AURKB (Aurora Kinase B) • CASP3 (Caspase 3)
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NOTCH1 mutation • AURKB overexpression • NOTCH1 overexpression
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Aliqopa (copanlisib) • omipalisib (GSK2126458) • alisertib (MLN8237) • danusertib (PHA-739358)
6ms
STK11 Prevents Invasion Through STAT3/5 and FAK Repression in Cutaneous Melanoma. (PubMed, J Invest Dermatol)
Using inhibitors of STAT3/5 and FAK, we reverted the invasive phenotype in both BRAF and NRAS mutated cells. Our findings confirm an increased invasive phenotype upon STK11-inactivation in BRAF and NRAS-mutant cutaneous melanoma that can be targeted by STAT3/5 and FAK-inhibition.
Journal
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NRAS (Neuroblastoma RAS viral oncogene homolog) • STK11 (Serine/threonine kinase 11) • STAT3 (Signal Transducer And Activator Of Transcription 3)
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NRAS mutation • BRAF mutation • STK11 mutation • AURKB overexpression • NRAS mutation + BRAF mutation
9ms
AURKB promotes tumorigenesis and carboplatin resistance by regulating the ERK pathway in neuroblastoma cells. (PubMed, Int J Neurosci)
Additionally, AURKB overexpression could potentiate the invasion and the expression of MRP1 and Ki67, while suppresses apoptosis in SK-N-AS-R and IMR-32-R, whereas ERK inhibitor U0126 could reverse the phenomenon caused by AURKB overexpression. AURKB overexpression was strongly associated with poor prognosis and carboplatin resistant acquisition. Additionally, suppression of AURKB-ERK axis might be a potential therapy for carboplatin resistance in NB patients.
Journal
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AURKB (Aurora Kinase B)
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AURKB overexpression
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carboplatin