HSP90 inhibitor 17AAG causes apoptosis in ATRA-resistant acute promyelocytic leukemia cells

被引：11

作者：

Meyer, Paul N. ^{[1
]}

Roychowdhury, Shantanu ^{[1
]}

Kini, Ameet R. ^{[1
]}

Alkan, Serhan ^{[1
]}

机构：

[1] Loyola Univ, Med Ctr, Dept Pathol, Maywood, IL 60153 USA

来源：

LEUKEMIA RESEARCH | 2008年 / 32卷 / 01期

关键词：

acute promyelocytic leukemia; APL; 17AAG; heat shock protein; HSP90; apoptosis; therapy; geldanamycin;

D O I：

10.1016/j.leukres.2007.05.009

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The effects of a novel heat shock protein inhibitor, 17AAG, on established APL cell lines (NB4 and R1) were analyzed. 17AAG induces apoptosis in APL cell lines both sensitive (NB4) and resistant (R 1) to ATRA after 72 h of incubation. Apoptosis occurs by a mechanism different than ATRA-inediated response, as the cells do not undergo differentiation before apoptosis. Analysis of bax and bcl-2 shows that pro-apoptotic (bax) and anti-apoptotic (bcl-2) proteins are decreased in expression after incubation with 17AAG. We believe this data supports potential clinical use of agents that target HSP90 in APL patients failing conventional therapy. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：143 / 149

页数：7

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