Androgen induction of prostate cancer cell invasion is mediated by ezrin

doi:10.1074/jbc.M602237200

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Papers In Press, published online ahead of print July 26, 2006
J. Biol. Chem, 10.1074/jbc.M602237200
Submitted on March 9, 2006
Revised on July 26, 2006
Accepted on July 26, 2006

Androgen induction of prostate cancer cell invasion is mediated by ezrin

Yin-Choy Chuan, See-Tong Pang, Angel Cedazo-Minguez, Gunnar Norstedt, Åke Pousette, and Amilcar Flores-Morales

Department of Molecular Medicine and Surgery, Karolinska Hospital, Stockholm 17176

Corresponding Author: Amilcar.Flores{at}cmm.ki.se

Ezrin is a key signaling molecule that regulates cell survival, adhesion, and migration/ invasion. We have previously shown that ezrin is regulated by androgen in rat prostate and that its expression is increased in prostate cancer as well as in prostate intraepithelial neoplasia. We have used the androgen sensitive cell line LNCaP-FGC to functionally evaluate the role of ezrin in androgen-induced cell invasion. We found that androgen treatment induces ezrin expression in LNCaP-FGC cells, an effect that is inhibited by the androgen receptor antagonist, bicalutamide. In addition, androgen treatment induces the phosphorylation of ezrin in Thr567 and Tyr353 in a sequential manner. This is mediated through PKCa and Src tyrosine kinase, respectively. Androgen treatment induces the translocations of both PKCa and ezrin to the cell membrane and their association. Inhibition of ezrin function using siRNA or the overexpression of T567A and Y353F-ezrin mutants significantly reduces androgen-induced matrigel invasion but do not affect cell proliferation or cell adhesion. Matrigel invasion of androgen insensitive PCa cells: PC-3 and LNCaP-R is also dependent on ezrin. In summary, androgens regulate ezrin at transcriptional and posttranscriptional levels. Hormonal regulation of ezrin phosphorylation is required for androgen-induced cell invasion.

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