Chemotherapy induces Bcl-2 cleavage in lymphoid leukemic cell lines

被引：5

作者：

Fortney, JE ^{[1
]}

Hall, BM ^{[1
]}

Bartrug, L ^{[1
]}

Gibson, LF ^{[1
]}

机构：

[1] W Virginia Univ, Robert C Byrd Hlth Sci Ctr, Dept Pediat, Morgantown, WV 26506 USA

来源：

LEUKEMIA & LYMPHOMA | 2002年 / 43卷 / 11期

关键词：

Bcl-2; ALL; stromal cells; apoptosis; chemotherapy;

D O I：

10.1080/1042819021000033024

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Bcl-2 is the major anti-apoptotic protein evaluated in studies aimed at understanding programmed cell death. Recent work suggests that the biological activity of Bcl-2 is modulated by proteolytic cleavage, with a 23 kDa cleaved Bcl-2 product having pro-apoptotic activity. In the current study we evaluated the effect of chemotherapy on Bcl-2 cleavage in B lineage leukemic cell lines. JM-1, SUP-B15 and RS4 leukemic cell lines cleaved Bcl-2 to its 23 kDa form when exposed to the chemotherapeutic agents 1-beta-(D)-arabinofuranosyl-cytosine (Ara-C) or etoposide (VP-16). Chemotherapy induced Bcl-2 cleavage was blunted by inhibition of caspase activity. Co-culture of leukemic cells with bone marrow stromal cells during chemotherapy exposure resulted in reduced levels of 23 kDa Bcl-2 protein. These observations suggest that the bone marrow microenvironment may contribute to maintenance of residual leukemic disease during treatment by reducing generation of pro-apoptotic 23 kDa Bcl-2.

引用

页码：2171 / 2178

页数：8

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