FCX, an arylidene derivative, induces apoptosis in androgen receptor-selective prostate cancer cells.

<bold>Context: </bold>Rational screening of arylidene derivatives for biological activities has resulted in many lead molecules with anticancer properties with effective therapeutic window.<bold>Aims: </bold>In the current study, FCX, an arylidene derivative, was screened for anticolon and prostate cancer activity.<bold>Settings and Design: </bold>Prostate and colon cancer cell lines were used to check the FCX effect on proliferation, apoptosis, and mechanism of drug action.<bold>Subjects and Methods: </bold>LNCaP, PC-3, HCT-8, and HT-29 cells were treated with various concentrations of the FCX. MTT assay was performed to check proliferation, propidium iodide and Hoechst dual staining for DNA fragmentation, and Annexin V binding assay for apoptosis, and cell cycle assay was done using flow cytometry. Functional androgen-mutated receptor cells were used mechanistic pathway elucidation.<bold>Statistical Analysis Used: </bold>A minimum of three individual replicates at different time periods were taken as mean value. The data were expressed in mean ± standard deviation. Student's t-test and one-way ANOVA were used to assess the statistical difference between the groups.<bold>Results: </bold>FCX inhibited proliferation of prostate cancer cell lines in a dose-dependent manner with more selectivity toward LNCaP cells. Nuclear fragmentation and dose-dependent increase in Annexin V-positive LNCaP cells revealed apoptosis. Cell cycle G2/M phase arrest along with sub-G0/G1 population augmented the antiproliferative observations. Addition of FCX in the presence of estradiol, testosterone, and dehydroepiandrosterone, LNCaP cells markedly caused a dose-dependent increase in cell proliferation indicating the compound activity to be facilitated through androgen receptor pathway.<bold>Conclusions: </bold>Together with the results, it is evident that FCX has a wide therapeutic window in the in vitro inhibition of the prostate cancer cells mediated by hormone-dependent effects. [ABSTRACT FROM AUTHOR]