miR-186 inhibits cell proliferation of prostate cancer by targeting GOLPH3.

Am J Cancer Res

Department of Pathology, Nanfang Hospital, Southern Medical UniversityGuangzhou, Guangdong, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical UniversityGuangzhou, Guangdong, China; Guangdong Provincial Key Laboratory of Molecular Tumor PathologyGuangzhou, Guangdong, China.

Published: September 2016

Prostate cancer is one of the leading causes of cancer deaths among men, many miRNAs have been demonstrated to play critical role in the progression of prostate cancer, miR-186 suppresses the progression of many tumors, such as bladder cancer and glioma. Previous study shows miR-186 is downregulated in prostate cancer tissues, and is a good prognosis for prostate cancer patients. In this study, we found miR-186 was downregulated in prostate cancer cells and tissues, overexpression of miR-186 inhibited cell proliferation and tumorigenesis in vitro determined by MTT assay, colony formation assay and soft agar growth assay, whereas knockdown of miR-186 reduced these effects. Cell cycle analysis found miR-186 overexpression arrested cell cycle in G0/G1 phase, and reduced p21 and p27 levels, and enhanced Cyclin D1 and the phosphorylation of Rb levels, suggesting miR-186 blocked G1/S transition. A novel oncogene Golgi phhosphoprotein 3 (GOLPH3) was the target of miR-186, miR-186 bound to the 3'UTR of GOLPH3. Moreover, miR-186 was negatively correlated with GOLPH3 in prostate cancer tissues. In conclusion, our study suggested miR-186 inhibited cell proliferation through targeting oncogene GOLPH3.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004070PMC

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