miR‑28‑3p inhibits prostate cancer cell proliferation, migration and invasion, and promotes apoptosis by targeting ARF6
- Jiabin Zhang
- Yi Yao
- Huizhang Li
- Shihua Ye
Affiliations: Department of Urology, Mindong Hospital Affiliated to Fujian Medical University, Ningde, Fujian 355000, P.R. China
- Published online on: August 24, 2021 https://doi.org/10.3892/etm.2021.10639
Copyright: © Zhang
et al. This is an open access article distributed under the
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Previous studies have reported that the expression levels of microRNA (miR)‑28‑3p are downregulated in prostate cancer (PCa) compared with those in adjacent normal tissues. However, to the best of our knowledge, the function and underlying mechanisms of miR‑28‑3p in PCa have not been reported. The present study aimed to explore the role of miR‑28‑3p and its mechanism in the development of PCa. In the present study, miR‑28‑3p and ADP‑ribosylation factor 6 (ARF6) expression levels were analyzed using reverse transcription‑quantitative PCR (RT‑qPCR). Cell proliferation, colony formation, apoptosis, migration and invasion were determined using Cell Counting Kit‑8, colony forming, flow cytometry and Transwell assays, respectively. The association between miR‑28‑3p and ARF6 was investigated using a dual luciferase reporter assay. ARF6, Rac1, Erk1/2 and phosphorylated (p)‑Erk1/2 protein expression levels were analyzed using western blotting. The results of the present study revealed that miR‑28‑3p expression levels were downregulated, whereas ARF6 expression levels were upregulated in PCa cell lines (LNCaP, 22Rv‑1, PC‑3 and DU145) compared with those in the normal prostate line RWPE‑1. The overexpression of miR‑28‑3p promoted cell apoptosis, and inhibited cell proliferation, colony formation, migration and invasion. However, the knockdown of miR‑28‑3p exerted the opposite results. The results of the dual luciferase reporter assays, RT‑qPCR and western blotting indicated that ARF6 was a target gene of miR‑28‑3p. Finally, rescue experiments demonstrated that ARF6 overexpression attenuated the effects of the miR‑28‑3p mimic by upregulating Rac1 and p‑Erk1/2 expression in PCa cells. In conclusion, these findings indicated that miR‑28‑3p may inhibit the biological ehaviors of PCa cells by targeting ARF6, and therefore may represent a novel therapeutic candidate for PCa.