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Anti‐proliferative effect of a triazole derivative (ST1959) on LNCaP human prostate cancer cells through down‐regulation of cyclin and androgen receptor expression
Author(s) -
Loiarro Maria,
Campo Silvia,
Arseni Brunilde,
Rossi Stefania,
D'Alessio Valeria,
De Santis Rita,
Sette Claudio,
Ruggiero Vito
Publication year - 2010
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.21219
Subject(s) - lncap , androgen receptor , cell growth , prostate cancer , cyclin d1 , androgen , cancer research , endocrinology , medicine , cyclin , prostate , biology , cell cycle , chemistry , cancer , biochemistry , hormone
Abstract BACKGROUND Previous studies demonstrated that ST1959, a triazole derivative endowed with immunomodulatory activities, also exerts inhibitory effects on proliferation and survival of a panel of tumor cells. In this study, we sought to ascertain the effects of ST1959 on the growth of androgen‐dependent and androgen‐independent prostate cancer (PCa) cells. METHODS The growth of androgen‐dependent (LNCaP) and androgen‐independent (PC3, DU‐145) cells was analyzed in vitro both in the presence and absence of ST1959. Modulation of cyclin and androgen receptor (AR) expression following treatment with ST1959 was analyzed by Western blot and cytofluorimetric analysis. RESULTS We observed that ST1959 causes a significant growth inhibition of LNCaP cells without affecting proliferation of androgen‐insensitive DU‐145 and PC3 cell lines. These effects were associated with G0/G1 cell cycle arrest and down‐regulation of cyclin D1, A and B and AR expression. CONCLUSIONS Our present findings indicate that the anti‐proliferative activity of ST1959 on cell growth of androgen‐dependent LNCaP PCa cells may be brought about by decreasing expression of functional AR and selected cyclins, ultimately leading to cell growth inhibition. Prostate 71: 32–41, 2011. © 2010 Wiley‐Liss, Inc.