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Combined Treatment With ABT-737 and VX-680 Induces Apoptosis in Bcl-2- And c-FLIP-overexpressing Breast Carcinoma Cells

Combined Treatment With ABT-737 and VX-680 Induces Apoptosis in Bcl-2- And c-FLIP-overexpressing Breast Carcinoma Cells

Jung Eun Choi, Seon Min Woo, Kyoung-Jin Min, Su Hwan Kang, Soo Jung Lee, Taeg Kyu Kwon

Oncol Rep. 2015 Mar;33(3):1395-401.

PMID: 25592064

Abstract:

ABT-737, a BH3-mimetic small-molecule inhibitor, binds with very high affinity to Bcl-2, Bcl-xL and Bcl-w, and inhibits their activity. Aurora kinase is one of the serine/threonine kinase family members and is a vital and critical regulator of mitosis and meiosis. In the present study, we investigated the effects and mechanisms of a combined treatment of ABT-737 and VX-680 (Aurora kinase inhibitor) in human breast cancer MDA-MB‑435S cells. ABT-737 plus VX-680 induced caspase-dependent apoptosis in the human breast cancer cells. Combined treatment with ABT-737 and VX-680 led to the downregulation of Bcl-2 expression at the transcriptional level and the downregulation of c-FLIP and Mcl-1 expression at the post-transcriptional level. Overexpression of Bcl-2 or c-FLIP could not block the induction of apoptosis caused by the combined treatment with ABT-737 and VX-680. However, overexpression of Mcl-1 partially inhibited the induction of apoptosis. In contrast, the combined treatment with ABT-737 and VX680 had no effect on the apoptosis in normal cells. Taken together, our study demonstrated that combined treatment with ABT-737 and VX-680 induced apoptosis in anti‑apoptotic protein (Bcl-2 or c-FLIP)-overexpressing cells.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP639089546	VX-680		639089-54-6	Price

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