The heat shock protein 90 inhibitor 17-AAG induces cell cycle arrest and apoptosis in mantle cell lymphoma cell lines by depleting cyclin D1, Akt, Bid and activating caspase 9

被引：69

作者：

Georgakis, Georgios V. ^{[1
]}

Li, Yang ^{[1
]}

Younes, Anas ^{[1
]}

机构：

[1] Univ Texas, MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Houston, TX 77030 USA

来源：

BRITISH JOURNAL OF HAEMATOLOGY | 2006年 / 135卷 / 01期

关键词：

lymphoma; apoptosis; geldanamycin;

D O I：

10.1111/j.1365-2141.2006.06247.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Mantle cell lymphoma (MCL), a distinct type of non-Hodgkin lymphoma, is characterised by the overexpression of cyclin D1. Heat shock protein 90 (HSP90) is a molecular chaperon to proteins that regulate cell cycle and survival. 17-allylamino-17-demethoxy-geldanamycin (17-AAG), a HSP90 small molecule inhibitor, induced G(0/1) cell cycle arrest and cell death in a dose- and time-dependent manner in MCL cell lines. This effect was associated with the downregulation of cyclin D1, cdk4 and Akt, depletion of Bid, and activation of the intrinsic/mitochondrial caspase pathway. These data suggest that 17-AAG may have a potential therapeutic value in patients with MCL.

引用

页码：68 / 71

页数：4

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