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鉴定 microRNA-132 及其靶基因在前列腺癌肿瘤发生中的肿瘤抑制作用。

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

机构信息

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.

出版信息

Int J Mol Med. 2018 Apr;41(4):2429-2433. doi: 10.3892/ijmm.2018.3421. Epub 2018 Jan 23.

DOI:10.3892/ijmm.2018.3421
PMID:29393367
Abstract

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.

摘要

先前的文献研究了 microRNA(miR)-132 在各种恶性肿瘤的发生和发展中的作用。在本研究中,我们旨在了解 miR-132 与前列腺肿瘤发生之间的关系。我们收集了 32 例前列腺癌组织和相邻的非癌对照组织,检测了 miR-132 的表达水平。然后在网上搜索 miRNA 数据库并进行荧光素酶检测,以了解 miR-132 与 E2F5 之间的调控关系。此外,我们还通过实时 PCR 和 Western blot 分析研究了不同组(癌组织,n=32;非癌组织,n=32)或用 scramble 对照、miR-132 模拟物、E2F5 siRNA 和 miR-132 抑制剂处理的细胞中 E2F5 的 mRNA 和蛋白表达水平。miR-132 在前列腺癌患者的癌组织中上调。E2F5 是 miR-132 的靶基因,荧光素酶检测也证实了 miR-132 与 E2F5 之间存在负向调控关系。癌组织组中 E2F5 的 mRNA 和蛋白表达水平增加。miR-132 降低前列腺癌细胞中 E2F5 的表达,引入 miR-132 降低了前列腺癌细胞的活力并促进了其活力。miR-132 抑制细胞凋亡,而 E2F5 加速细胞凋亡。总之,miR-132 在前列腺癌癌组织中上调。E2F5 是 miR-132 的直接靶基因,miR-132 上调导致 E2F5 下调可能有助于前列腺癌的发生。

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