Regulation of protein kinase C δ by estrogen in the MCF-7 human breast cancer cell line

被引:46
作者
Shanmugam, M
Krett, NL
Maizels, ET
Cutler, RE
Peters, CA
Smith, LM
O'Brien, ML
Park-Sarge, OK
Rosen, ST
Hunzicker-Dunn, M
机构
[1] Northwestern Univ, Sch Med, Dept Cell & Mol Biol, Chicago, IL 60611 USA
[2] Northwestern Univ, Sch Med, Dept Med, Chicago, IL 60611 USA
[3] Northwestern Univ, Sch Med, Robert H Lurie Canc Ctr, Chicago, IL 60611 USA
[4] Univ Kentucky, Coll Med, Dept Physiol, Lexington, KY 40536 USA
关键词
estrogen; PKC delta; breast cancer; signal transduction;
D O I
10.1016/S0303-7207(98)00229-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
We have previously shown that estrogen up-regulates expression of protein kinase C (PKC) delta in the rat and rabbit corpus luteum as well as in luteinized rat granulosa primary cell cultures. To determine whether a similar regulation of the PKC delta isoform by estrogen occurred in another estrogen responsive system, we investigated the estrogen receptor positive MCF-7 human breast cancer cells. In a characterization of PKC isoforms in MCF-7 cells we determined that PKC delta was the predominant PKC isoform. However in contrast to the effect of estrogen on PKC delta expression in ovarian cells, estrogen treatment of MCF-7 cells resulted in a significant decrease in PKC delta protein and mRNA expression in a time and dose dependent manner. Treatment of MCF-7 cells with 10(-10)-10(-8) M estrogen for 7 days down-regulated specifically PKC delta mRNA and protein while expression of other PKC isoforms was unchanged. The opposite regulation of PKC 6 expression in ovarian and breast cancer cells prompted us to evaluate the type of estrogen receptor present in both cell types. Results showed that luteinized I-at granulosa cells expressed predominantly estrogen receptor beta while the MCF-7 cells expressed predominantly estrogen receptor alpha and barely detectable levels be a result of differential signaling through the two estrogen receptor subtypes. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:109 / 118
页数:10
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