BCL-2 family regulation by the 20S proteasome inhibitor bortezomib

被引：129

作者：

Fennell, D. A. ^{[1
]}

Chacko, A. ^{[1
]}

Mutti, L. ^{[2
]}

机构：

[1] Queens Univ Belfast, Thorac Oncol Res Grp, Ctr Canc Res & Cell Biol, Belfast, Antrim, North Ireland

[2] Med Gen Lab Oncol Clin, Vercelli, Italy

来源：

ONCOGENE | 2008年 / 27卷 / 09期

关键词：

mitochondria; proteasome; BAX; BAK; BIM; NOXA;

D O I：

10.1038/sj.onc.1210744

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Bortezomib (Velcade, PS341) was licensed in 2003 as a first-in-class 20S proteasome inhibitor indicated for treatment of multiple myeloma, and is currently being evaluated clinically in a range of solid tumours. The mechanisms underlying its cancer cell toxicity are complex. A growing body of evidence suggests proteasome inhibition-dependent regulation of the BCL-2 family is a critical requirement. In particular, the stabilization of BH3-only proteins BIK, NOXA and BIM, appear to be essential for effecting BAX- and BAK-dependent cell death. These mechanisms are reviewed and the implications for favourable novel drug interactions are highlighted.

引用

页码：1189 / 1197

页数：9

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