Pinocembrin flavanone inhibits cell viability in PC-3 human prostate cancer by inducing cellular apoptosis, ROS production and cell cycle arrest.

The main purpose of the present study was to evaluate the antitumor effects of pinocembrin in human prostate cancer cells (PC-3) along with investigating its effects on cell apoptosis, endogenous ROS production and cell cycle. MTT assay and clonogenic assays were used to study the effects on cell viability and cancer colony formation, respectively. Fluorescence microscopy along with Western blotting was used to study apoptotic effects induced by pinocembrin. Flow cytometry was used to study effects on ROS production and cell cycle phase distribution. Results indicated that pinocembrin promoted inhibition cell proliferation along with reducing cancer colony formation of PC-3 cells in a dose-dependent manner. Pinocembrin induced regulatory effects over expressions of caspase-3, caspase-9, Bax and Bcl-2, thereby promoting apoptotic cell death in PC-3 cells. It also led to the dose-dependent G0/G1 cell cycle arrest. In conclusion, pinocembrin exhibits strong anticancer effects in human prostate cancer cells mediated via apoptosis, endogenous ROS production and G0/G1 cell cycle arrest.

MicroRNA-501-3p restricts prostate cancer growth through regulating cell cycle-related and expression-elevated protein in tumor/cyclin D1 signaling.

MicroRNA-501-3p (miR-501-3p) has been reported as a novel cancer-related miRNA in many types of cancer. However, the precise biological function of miR-501-3p in prostate cancer remains unknown. In this study, we aimed to investigate the regulatory effect and mechanism of miR-501-3p on cell growth of prostate cancer cells. We found that miR-501-3p expression was significantly downregulated in prostate cancer tissues and cell lines. Gain-of-function experiments showed that upregulation of miR-501-3p expression significantly decreased cell proliferation and colony formation, and induced cell cycle arrest in the G0/G1 phase. Bioinformatics analysis predicted that cell cycle-related and expression-elevated protein in tumor (CREPT) was a potential target gene of miR-501-3p., and the results of our luciferase reporter assay confirmed that miR-501-3p bound to the 3'-untranslated region of CREPT at the predicted binding site. Moreover, miR-501-3p was shown to negatively regulate CREPT expression in prostate cancer cells. Correlation analysis showed that miR-501-3p was inversely correlated with CREPT expression in prostate cancer tissues. Knockdown studies revealed that miR-501-3p regulated the expression of cyclin D1 by targeting CREPT. Additionally, the inhibitory effect of miR-501-3p on prostate cancer cell growth was partially reversed by CREPT overexpression. Overall, these results suggest that miR-501-3p restricts prostate cancer cell growth by targeting CREPT to inhibit the expression of cyclin D1. These findings indicate that the miR-501-3p/CREPT/cyclin D1 axis plays a crucial role in the progression of prostate cancer and may serve as potential therapeutic target.