BH3 mimetics to improve cancer therapy; mechanisms and examples

被引：128

作者：

Zhang, Lin ^{[1
,2
]}

Ming, Lihua ^{[1
,2
]}

Yu, Han ^{[1
,2
]}

机构：

[1] Univ Pittsburgh, Pittsburgh Canc Inst, Hillman Canc Ctr, Sch Med,Dept Pharmacol, Pittsburgh, PA 15213 USA

[2] Univ Pittsburgh, Pittsburgh Canc Inst, Hillman Canc Ctr, Sch Med,Dept Pathol, Pittsburgh, PA 15213 USA

来源：

DRUG RESISTANCE UPDATES | 2007年 / 10卷 / 06期

关键词：

apoptosis; cancer; drug resistance; BH3; mimetic; ABT-737;

D O I：

10.1016/j.drup.2007.08.002

中图分类号：

R9 [药学];

学科分类号：

1007 [药学];

摘要：

Tumor cell survival is highly dependent on the expression of certain pro-survival Bcl-2 family proteins. An attractive therapeutic approach is to inhibit these proteins using agents that mimic the Bcl-2 homology 3 (BH3) domains of the proapoptotic Bcl-2 family members, which neutralize these proteins by binding to their surface hydrophobic grooves. A number of BH3 mimetic peptides and small molecules have been described, a few of which have advanced into clinical trials. Recent studies have highlighted ABT-737, a bona fide BH3 mimetic and potent inhibitor of antiapoptotic Bcl-2 family members, as a promising anticancer agent. This review summarizes recent advances in understanding the mechanisms of action of BH3 domains and several classes of BH3 mimetics, as well as the prospects of using these agents to improve cancer therapy. (c) 2007 Elsevier Ltd. All rights reserved.

引用

收藏

页码：207 / 217

页数：11

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