MicroRNA‑16‑5p regulates cell survival, cell cycle and apoptosis by targeting AKT3 in prostate cancer cells

Oncol Rep. 2020 Sep;44(3):1282-1292. doi: 10.3892/or.2020.7682. Epub 2020 Jul 9.

Abstract

Prostate cancer (PCa) is a malignancy with the highest morbidity rate in 105 countries worldwide and was a major cause of cancer‑associated death in men in 2018. Accumulating evidence suggests that microRNAs (miRNAs/miRs) have important functions in the carcinogenesis of PCa, and may provide novel treatment targets. Previous studies have indicated that miR‑16‑5p is associated with PCa. However, the relevance and importance of miR‑16‑5p in PCa carcinogenesis are still not completely understood. In the current study, we aimed to investigate the role and mechanism of miR‑16‑5p in PCa carcinogenesis. The results showed that miR‑16‑5p was markedly downregulated in PCa cells, and MTS assay, colony formation, flow cytometric analyses demonstrated that miR‑16‑5p inhibited PCa cell survival, regulated cell cycle distribution and induced apoptosis. Moreover, luciferase reporter assay and western blot analysis showed that miR‑16‑5p directly targets AKT3 (AKT serine/threonine kinase 3), which is associated with PCa carcinogenesis, and the effects of the downregulation of AKT3 were similar to the effects of upregulation of miR‑16‑5p in PC‑3 cells. In conclusion, our data clarify that miR‑16‑5p has anticancer functions in PCa cells, and our findings provide experimental evidence to highlight the potential value of miR‑targeting treatment strategies for PCa.

Keywords: microRNA-16-5p; cell survival; cell cycle; apoptosis; prostate cancer.

MeSH terms

  • Apoptosis / genetics
  • Carcinogenesis / genetics*
  • Cell Cycle / drug effects
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / genetics
  • Computational Biology
  • Datasets as Topic
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Male
  • MicroRNAs / agonists
  • MicroRNAs / metabolism*
  • Prostate / pathology
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology
  • Proto-Oncogene Proteins c-akt / genetics*

Substances

  • MIRN16 microRNA, human
  • MicroRNAs
  • AKT3 protein, human
  • Proto-Oncogene Proteins c-akt