INTERLEUKIN-7 INHIBITS APOPTOSIS OF MOUSE MALIGNANT T-LYMPHOMA CELLS BY BOTH SUPPRESSING THE CPP32-LIKE PROTEASE ACTIVATION AND INDUCING THE BCL-2 EXPRESSION
Sh. Lee et al., INTERLEUKIN-7 INHIBITS APOPTOSIS OF MOUSE MALIGNANT T-LYMPHOMA CELLS BY BOTH SUPPRESSING THE CPP32-LIKE PROTEASE ACTIVATION AND INDUCING THE BCL-2 EXPRESSION, Oncogene, 13(10), 1996, pp. 2131-2139
Mouse malignant T-lymphoma CS-21 cells grow in vitro in the presence o
f CA-12 lymph node stromal cells, but they undergo apoptotic cell deat
h 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 apopt
osis, 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 res
ults 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.