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Ref Type Journal Article
PMID (28179288)
Authors Murai S, Matuszkiewicz J, Okuzono Y, Miya H, DE Jong R
Title Aurora B Inhibitor TAK-901 Synergizes with BCL-xL Inhibition by Inducing Active BAX in Cancer Cells.
Journal Vol Issue Date Pages Journal Short Title
Anticancer research 37 2 2017 02 437-444 Anticancer Res
URL
Abstract Text Aurora B kinase plays an essential role in chromosome segregation and cytokinesis, and is dysregulated in many cancer types, making it an attractive therapeutic target. TAK-901 is a potent aurora B inhibitor that showed efficacy in both in vitro and in vivo oncology models.We conducted a synthetic lethal siRNA screening to identify the genes that, when silenced, can potentiate the cell growth-inhibitory effect of TAK-901.B-cell lymphoma-extra large (BCL-xL) depletion by siRNA or chemical inhibition synergized with TAK-901 in cancer cell lines. As a mechanism of synthetic lethality, active BCL2 associated X, apoptosis regulator (BAX) was induced by TAK-901. BCL-xL protected cells from BAX-dependent apoptosis induction. Therefore, TAK-901 sensitizes cancer cells to BCL-xL inhibition.Polyploid cells induced by TAK-901 are vulnerable to BCL-xL inhibition. Our findings may have an impact on combination strategies with aurora B inhibitors in clinical studies.

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Molecular Profile Treatment Approach
Gene Name Source Synonyms Protein Domains Gene Description Gene Role
Therapy Name Drugs Efficacy Evidence Clinical Trials
TAK-901 TAK-901 0 0
Drug Name Trade Name Synonyms Drug Classes Drug Description
TAK-901 Aurkb Inhibitors 21 FGFR2 Inhibitor 23 FLT3 Inhibitor 66 TAK-901 is a selective inhibitor of Aurora B kinase, FLT3, and FGFR2, and has demonstrated anti-tumor activity in several cancer models (PMID: 23358665, PMID: 28179288).
Gene Variant Impact Protein Effect Variant Description Associated with drug Resistance
Molecular Profile Indication/Tumor Type Response Type Therapy Name Approval Status Evidence Type Efficacy Evidence References