Prolactin-regulated apoptosis of Nb2 lymphoma cells -: pim-1, bcl-2, and bax expression

被引:58
作者
Krumenacker, JS
Buckley, DJ
Leff, MA
McCormack, JT
de Jong, G
Gout, PW
Reed, JC
Miyashita, T
Magnuson, NS
Buckley, AR
机构
[1] Univ N Dakota, Dept Pharmacol & Toxicol, Sch Med & Hlth Sci, Grand Forks, ND 58201 USA
[2] Univ N Dakota, Dept Anat & Cell Biol, Sch Med & Hlth Sci, Grand Forks, ND 58201 USA
[3] British Columbia Canc Agcy, Dept Med Oncol, Vancouver, BC V5Z 4E6, Canada
[4] British Columbia Canc Agcy, Dept Canc Epidemiol, Vancouver, BC V5Z 4E6, Canada
[5] Burnham Inst, La Jolla, CA 92037 USA
[6] Washington State Univ, Dept Microbiol, Pullman, WA 99164 USA
关键词
apoptosis; dexamethasone; prolactin; Nb2; cells;
D O I
10.1385/ENDO:9:2:163
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Lactogen-dependent Nb2 lymphoma cells, widely employed for studying prolactin (PRL) mitogenic mechanisms, are also useful for investigations of apoptosis in T-lineage lymphocytes, Utilizing PRL-dependent Nb2-11 cultures, apoptosis-regulatory genes were evaluated for participation in dexamethasone- (DE);) provoked cell death or its inhibition by PRL, Treatment of lactogen-starved, G(1)-arrested Nb2-11 cells with DEX (100 nM) activated apoptosis within 12 h evaluated by flow cytometric analysis of fragmented DNA, This effect was not associated with altered expression of bcl-2, bax, or pim-1. PRL (10 ng/mL), coincubated with DEX-treated cells, completely blocked DEX-induced apoptosis. This inhibition was associated with increased expression of bcl-2 anal pim-1 mRNAs, genes reported to suppress apoptosis, within 2-6 h after addition of the hormone. Moreover, the increased transcription of bcl-2 and pim-1 was coupled to increases in their protein levels. The results suggest that bcl-2, bax, and pim-1 do not play a critical role in DEX-induced apoptosis in Nb2 cells. However, expression of bcl-2, together with pim-1, may have a role in mediating the antiapoptotic actions of PRL.
引用
收藏
页码:163 / 170
页数:8
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