Abstract
BackgroundArsenic trioxide (As2O3) as an inorganic compound is used to treat various cancers and other diseases. It has been reported that arsenic trioxide induced cellular apoptosis in certain kinds of cancers, including prostate cancers. The present study aimed to elucidate the crucial cooperative role of arsenic trioxide and Curcumin and their ability to protect against prostate cancers by targeting the epithelial-to-mesenchymal transition and expression of apoptosis-related genes. Material and methodsThe human prostate cell lines (LNCaP and PC3) were treated with different concentrations of Curcumin and As2O3 alone and combined to find effective doses and IC50 values. Percentages of apoptotic cells were evaluated by Annexin/P.I. staining, the proliferative inhibitory effect was assessed by Micro Culture Tetrazolium Test (MTT), and mRNA levels of KLK2, E-cadherin, SNAIL, angiogenesis genes (VEGFA and VEGFC), and apoptosis genes (BAX, Bcl2, and P53) expression were investigated by the real-time PCR method. ANOVA and t-test were used to appraise the results. ResultsFor the first time, we presented that the combination therapy of Curcumin and As2O3 increases prostate cancer cell apoptosis and inhibits proliferation; Our data displayed that Curcumin (15 μM and 10 μM in PC3 and LNCap), As2O3 (8 μM and 5 μM in PC3 and LNCap), and also their combination (15 μM Curcumin and 8 μM As2O3 in PC3, 10 μM Curcumin and 5 μM As2O3 in LNCap cell lines) significantly increased the percentage of apoptotic cells and inhibited cell growth (P < 0.05) compared with each drug alone. Generally, both cell lines treated with the combination of Curcumin and As2O3 displayed decreased angiogenesis genes (VEGFA and VEGFC), apoptosis genes (BAX and Bcl2), and prostate cancer marker (KLK2), the zinc-finger protein (SNAIL); and an increase in expression (P < 0.05) of cell–cell adhesion molecule (E-cadherin) and tumor suppressor gene (P53) genes. ConclusionsThe antitumor effects of combination therapy with As2O3 and Curcumin have been displayed on prostate cancer cell lines (LNCaP and PC3), which probably originates from their potential to induce apoptosis and inhibit the growth of prostate cancer cells simultaneously.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.