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

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 t...

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Veröffentlicht in:Oncology reports 2020-09, Vol.44 (3), p.1282-1292
Hauptverfasser: Wang, Fang, Wang, Wendi, Lu, Lina, Xie, Yi, Yan, Junfang, Chen, Yuhong, Di, Cutxia, Gan, Lu, Si, Jing, Zhang, Hong, Mao, Aihong
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Sprache:eng
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Zusammenfassung: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 investigatethe role and mechanism of miR-16-5p in PCa carcinogenesis. The results showed that miR-16-5p was markedly downregulatedin 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 downregula-tion of AKT3 were similar to the effects of upregulation of miR-16-5p in PC-3 cells. In conclusion, our data clarify that miR-16-5phas anticancer functions in PCa cells, and our findings provide experimental evidence to highlight the potential value of miR-targeting treatment strategies for PCa.
ISSN:1021-335X
1791-2431
DOI:10.3892/or.2020.7682