Previous literature exists on the role of microRNA (miR)-132 in initiation and progression of various malignancies. In this study, we aimed at understanding the relationship of miR-132 of prostate tumorigenesis. We collected 32 prostate cancer tissues and adjacent non-cancerous controls, and detected the expression level of miR-132. Then the miRNA database was searched online and luciferase assay perform to understand the regulatory relationship between miR-132 and E2F5. Moreover, we also conducted real-time PCR and western blot analysis to study the mRNA and protein expression level of E2F5 among different groups (cancerous tissue, n=32; non-cancerous tissue, n=32) or cells treated with scramble control, miR-132 mimics, E2F5 siRNA and miR-132 inhibitors. miR-132 was upregulated in cancerous tissues of prostate cancer patients. E2F5 was the target of miR-132, and negative regulatory relationship between miR-132 and E2F5 was also confirmed by luciferase assay. The mRNA and protein expression level of E2F5 increased in cancerous tissue group. miR-132 decreased the expression of E2F5 in prostate cancer cells, and introduction of miR-132 reduced the viability and E2F5 and promoted the viability of prostate cancer cells. miR-132 inhibited apoptosis and E2F5 accelerated apoptosis. In conclusion, miR-132 was upregulated in cancerous tissue of prostate cancer. E2F5 was a direct target of miR-132, and downregulation of E2F5 caused by upregulation of miR-132 may contribute to the tumorigenesis of prostate cancer.
International journal of molecular medicine. 2018 Jan 23 [Epub ahead of print]
Shun-Lai Li, Ying Sui, Jie Sun, Ting-Qi Jiang, Gang Dong
Department of Urology, The Fifth People's Hospital of Jinan, Jinan, Shandong 250012, P.R. China., Tianqiao Hospital in Jinan of Shandong, Jinan, Shandong 250022, P.R. China.