Protein kinase C ε mediates the induction of P-glycoprotein in LNCaP prostate carcinoma cells

被引：27

作者：

Flescher, E ^{[1
]}

Rotem, R ^{[1
]}

机构：

[1] Tel Aviv Univ, Sch Med, Sackler Fac Med, Dept Human Microbiol, IL-69978 Tel Aviv, Israel

来源：

CELLULAR SIGNALLING | 2002年 / 14卷 / 01期

关键词：

PKC; P-glycoprotein; prostate; aspirin; multidrug resistance; MDR;

D O I：

10.1016/S0898-6568(01)00215-7

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

P-glycoprotein (P-gp) mediates drug resistance. Protein kinase C (PKC) expression correlates with drug resistance in several types of cancer. We determined whether PKC signals the induction of P-gp in LNCaP human prostate cancer cells, and identified a specific isozyme involved, in a model of aspirin-induced P-glycoprotein expression. An inhibitor of PKC activity, and a specific peptide inhibitor of PKC epsilon translocation, suppressed the induction of P-gp. The PKC activator ingenol, but not OAG, induced P-gp expression in a dose-dependent manner. Based on our results, we conclude that PKC epsilon mediates the induction of P-gp. Accordingly, PKC epsilon is activated and translocates from the membrane fraction to the cytoskeleton fraction in aspirin-treated cells. The findings of this study point to PKC epsilon as a signalling molecule for the induction of P-gp in LNCaP prostate cancer cells. (C) 2002 Elsevier Science Inc. All rights reserved.

引用

页码：37 / 43

页数：7

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