Effects of miR‑129‑3p on biological functions of prostate cancer cells through targeted regulation of Smad3
- Yunpeng Jia
- Yu Gao
- Jianguo Dou
Affiliations: Department of Urology Surgery, Gansu Provincial Hospital of TCM, Lanzhou, Gansu 730050, P.R. China, Department of Urology Surgery, The Dazu District People's Hospital, Chongqing 402360, P.R. China
- Published online on: December 13, 2019 https://doi.org/10.3892/ol.2019.11216
Copyright: © Jia
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Effects of miR‑129‑3p on the biological functions of prostate cancer cells through the targeted regulation of Smad3 were investigated. RT‑PCR was used to detect the expression levels of miR‑129‑3p in prostate cancer tissues and cells and its target gene Smad3 mRNA determined by bioinformatics prediction. Correlation between miR‑129‑3p and Smad3 was analyzed. MTT assay, cell invasion detection, and apoptosis detection were conducted to detect the effects of miR‑129‑3p and Smad3 on the proliferation, invasion, and apoptosis of prostate cancer cells. The results of RT‑qPCR showed that the expression level of miR‑129‑3p decreased but that of Smad3 increased in the prostate cancer tissue, and the expression levels of the two were significantly and negatively correlated. Additionally, the expression levels were closely related to the degree of tumor differentiation, TNM staging, and lymph node metastasis (P<0.05). Bioinformatics prediction and subsequent experiments proved that Smad3 was the direct target gene of miR‑129‑3p. Cell detection confirmed that the overexpression of miR‑129‑3p or the inhibition of Smad3 expression inhibited the proliferation and invasion of prostate cancer cells, promoting apoptosis, and increased the expression level of pro‑apoptotic protein Bax, as well as decreased the expression level of anti‑apoptotic protein Bcl‑2. Inhibition of miR‑129‑3p expression had the opposite effect to overexpression. miR‑129‑3p, which may be a new and potential target for the treatment of prostate cancer, can inhibit the proliferation and invasion of prostate cancer cells and promote their apoptosis by directly targeting Smad3.