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

被引：130

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

共 128 条

[21] A novel orally active proteasome inhibitor induces apoptosis in multiple myeloma cells with mechanisms distinct from Bortezomib [J].

Chauhan, D ;

Catley, L ;

Li, GL ;

Podar, K ;

Hideshima, T ;

Velankar, M ;

Mitsiades, C ;

Mitsiades, N ;

Yasui, H ;

Letai, A ;

Ovaa, H ;

Berkers, C ;

Nicholson, B ;

Chao, TH ;

Neuteboom, STC ;

Richardson, P ;

Palladino, MA ;

Anderson, KC .

CANCER CELL, 2005, 8 (05) :407-419

[22] Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function [J].

Chen, L ;

Willis, SN ;

Wei, A ;

Smith, BJ ;

Fletcher, JI ;

Hinds, MG ;

Colman, PM ;

Day, CL ;

Adams, JM ;

Huang, DCS .

MOLECULAR CELL, 2005, 17 (03) :393-403

[23] Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing bak activation and bax translocation [J].

Chen, Shuang ;

Dai, Yun ;

Harada, Hisashi ;

Dent, Paul ;

Grant, Steven .

CANCER RESEARCH, 2007, 67 (02) :782-791

[24] Bax-independent inhibition of apoptosis by Bcl-x(L) [J].

Cheng, EHY ;

Levine, B ;

Boise, LH ;

Thompson, CB ;

Hardwick, JM .

NATURE, 1996, 379 (6565) :554-556

[25] UBIQUITIN DEPENDENCE OF SELECTIVE PROTEIN-DEGRADATION DEMONSTRATED IN THE MAMMALIAN-CELL CYCLE MUTANT TS85 [J].

CIECHANOVER, A ;

FINLEY, D ;

VARSHAVSKY, A .

CELL, 1984, 37 (01) :57-66

[26] Mcl-1 interacts with truncated bid and inhibits its induction of cytochrome c release and its role in receptor-mediated apoptosis [J].

Clohessy, JG ;

Zhuang, JG ;

de Boer, J ;

Gil-Gómez, G ;

Brady, HJM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (09) :5750-5759

[27] Apoptosis induced by proteasome inhibition in cancer cells:: predominant role of the p53/PUMA pathway [J].

Concannon, C. G. ;

Koehler, B. F. ;

Reimertz, Claus ;

Murphy, B. M. ;

Bonner, C. ;

Thurow, N. ;

Ward, M. W. ;

Villunger, A. ;

Strasser, A. ;

Koegel, D. ;

Prehn, J. H. M. .

ONCOGENE, 2007, 26 (12) :1681-1692

[28] Cell cycle-dependent cytotoxic and cytostatic effects of bortezomib on colon carcinoma cells [J].

Coquelle, A ;

Mouhamad, S ;

Pequignot, MO ;

Braun, T ;

Carvalho, G ;

Vivet, S ;

Métivier, D ;

Castedo, M ;

Kroemer, G .

CELL DEATH AND DIFFERENTIATION, 2006, 13 (05) :873-875

[29] Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition [J].

Du, CY ;

Fang, M ;

Li, YC ;

Li, L ;

Wang, XD .

CELL, 2000, 102 (01) :33-42

[30] In vitro cytotoxic effect of proteasome inhibitor bortezomib in combination with purine nucleoside analogues on chronic lymphocytic leukaemia cells [J].

Duechler, M ;

Linke, A ;

Cebula, B ;

Shehata, M ;

Schwarzmeier, JD ;

Robak, T ;

Smolewski, P .

EUROPEAN JOURNAL OF HAEMATOLOGY, 2005, 74 (05) :407-417

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