Interleukin-7 inhibits apoptosis of mouse malignant T-lymphoma cells by both suppressing the CPP32-like protease activation and inducing the Bcl-2 expression

被引:0
|
作者
Lee, SH
Fujita, N
Mashima, T
Tsuruo, T
机构
[1] UNIV TOKYO,INST MOL & CELLULAR BIOSCI,BIOMED RES LAB,BUNKYO KU,TOKYO 113,JAPAN
[2] JAPANESE FDN CANC RES,CTR CANC CHEMOTHERAPY,TOSHIMA KU,TOKYO 170,JAPAN
关键词
interleukin-7; Bcl-2; ICE-family proteases; apoptosis; T-lymphoma;
D O I
暂无
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
Mouse malignant T-lymphoma CS-21 cells grow in vitro in the presence of CA-12 lymph node stromal cells, but they undergo apoptotic cell death when separated from CA-12 stromal cells. In the course of examining the nursing effects of CA-12 stromal cells, we found that these cells provided some soluble factors that suppressed CS-21 cell apoptosis. We recently found that cysteine was an antiapoptotic soluble factor. In this report, we identify interleukin-7 (IL-7) as another antiapoptotic soluble factor secreted by CA-12 stromal cells. Although the activity of CPP32-like protease was increased in induction of CS-21 cell apoptosis, the addition of IL-7 suppressed the activity. The expression of Bcl-2 protein was down-regulated when CS-21 cells were cultured alone, but the addition of IL-7 recovered the expression of Bcl-2. These results indicate that CA-12 stromal cells inhibit CS-21 cell apoptosis by producing IL-7, which leads to the suppression of CPP32-like protease activation and the expression of Bcl-2 protein.
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页码:2131 / 2139
页数:9
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