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ORIGINAL ARTICLE
Year : 2021  |  Volume : 17  |  Issue : 2  |  Page : 401-407

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


1 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia
2 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia; Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria, Egypt
3 Department of Microbiology and Parasitology, Center for Stem Cell Research, College of Medicine, King Khalid University, Abha, KSA

Correspondence Address:
Rajagopalan Prasanna
Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Khalid University, Abha
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcrt.JCRT_228_17

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Context: Rational screening of arylidene derivatives for biological activities has resulted in many lead molecules with anticancer properties with effective therapeutic window. Aims: In the current study, FCX, an arylidene derivative, was screened for anticolon and prostate cancer activity. Settings and Design: Prostate and colon cancer cell lines were used to check the FCX effect on proliferation, apoptosis, and mechanism of drug action. Subjects and Methods: 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. Statistical Analysis Used: 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. Results: 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. Conclusions: 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.


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