Identification of tumor suppressive role of microRNA-132 and its target gene in tumorigenesis of prostate cancer

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 detecte...

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Bibliographic Details
Published in:International journal of molecular medicine 2018-04, Vol.41 (4), p.2429-2433
Main Authors: Li, Shun-Lai, Sui, Ying, Sun, Jie, Jiang, Ting-Qi, Dong, Gang
Format: Article
Language:English
Subjects:
Apoptosis
Care and treatment
Cell cycle
Cell growth
Development and progression
Gene expression
Genetic aspects
Growth factors
Health aspects
MicroRNA
Prostate cancer
Studies
Thermal cycling
Transcription factors
Tumor suppressor genes
Tumorigenesis
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Summary: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.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2018.3421