Curcumin inhibits prostate cancer progression by regulating the miR-30a-5p/PCLAF axis

xlomafota13 shared this article with you from Inoreader Curcumin inhibits prostate cancer progression by regulating the miR-30a-5p/PCLAF axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Sep;22(3):969. doi: 10.3892/etm.2021.10401. Epub 2021 Jul 7. ABSTRACT Curcumin has been shown to inhibit the growth of a variety of tumor cells. However, the biological functions of curcumin in prostate cancer (PCa) have not yet fully elucidated. The objective of the present study was to investigate the role of curcumin on the proliferation, migration, invasion and apoptosis of PCa cells and the underlying mechanism. Cell Counting Kit-8 and flow cytometry were used to detect the effects of curcumin at different concentrations on the proliferation and apoptosis of PCa cell lines, PC-3 and DU145. BrdU and Transwell assays, western blotting and reverse transcription-quantitative PCR were used to determine the effect of curcumin on cell proliferation, migration and invasion, apoptosis-related protein expression, and microRNA (miR)-30a-5p and PCNA clamp associated factor (PCLAF) expression, respectively. In addition, bioi nformatics analysis and Pearson's correlation test were used to verify the relationship between miR-30a-5p and PCLAF. Curcumin was observed to impede the proliferation, migration and invasion of PCa cells, and promote their apoptosis in a time- and dose-dependent manner. Curcumin enhanced miR-30a-5p expression and inhibited PCLAF expression; furthermore, there was a negative correlation between miR-30a-5p and PCLAF expression in PCa tissues. In addition, transfection of miR-30a-5p inhibitors partially reversed the function of curcumin on cell proliferation, migration, invasion and apoptosis. Overall, curcumin suppressed the malignant biological behaviors of PCa cells by regulating the miR-30a-5p/PCLAF axis. PMID:34335911 | PM C:PMC8290411 | DOI:10.3892/etm.2021.10401 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.