Department of Urology, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, 050001, Hebei, China.
Second Department of Urology, Cangzhou Central Hospital, No. 16, Xinhua West Road, Cangzhou, 061001, Hebei, China.
Mamm Genome. 2021 Oct;32(5):371-380. doi: 10.1007/s00335-021-09874-4. Epub 2021 May 15.
Prostate cancer is not easy to metastasize because it is difficult to diagnose at an early stage, and there is no effective treatment currently. miRNA-217-5p has been reported to be a regulator in the process of prostate cancer. This study aimed to investigate how miRNA-217-5p affects the invasion and migration of prostate cancer. Luciferase assay was used to clarify whether the target gene Clusterin (CLU) was interacted directly with miR-217-5p. miR-217-5p and CLU were knocked down by transfecting respective siRNA into DU145 cells. The expression level of epithelial-mesenchymal transition (EMT)-related proteins was detected by Western blotting. Invasion and migration of DU145 cell were examined by wound healing assay. The results showed that miR-217-5p directly interacted with its target gene CLU, and the transfection of si-CLU and si-miR-217-5p had similar ability to regulate the expression level of EMT-related proteins, which in turn affected the migration and invasion of prostate cancer cell line DU145. In addition, miR-217-5p inhibited the expression of EMT-related proteins by regulating the expression of the target gene CLU, and further inhibited the invasion and migration of prostate cancer cells. Our findings provide a theoretical target basis for the treatment of prostate cancer.
前列腺癌不易转移,因为它在早期很难诊断,目前也没有有效的治疗方法。miRNA-217-5p 已被报道在前列腺癌的发生过程中起调节作用。本研究旨在探讨 miRNA-217-5p 如何影响前列腺癌的侵袭和迁移。荧光素酶报告基因实验用于阐明其靶基因 Clusterin (CLU) 是否与 miR-217-5p 直接相互作用。通过转染相应的 siRNA 到 DU145 细胞中敲低 miR-217-5p 和 CLU。通过 Western blot 检测上皮间质转化(EMT)相关蛋白的表达水平。通过划痕愈合实验检测 DU145 细胞的侵袭和迁移。结果表明,miR-217-5p 可直接与靶基因 CLU 相互作用,转染 si-CLU 和 si-miR-217-5p 具有相似的调节 EMT 相关蛋白表达水平的能力,进而影响前列腺癌细胞系 DU145 的迁移和侵袭。此外,miR-217-5p 通过调节靶基因 CLU 的表达抑制 EMT 相关蛋白的表达,进而抑制前列腺癌细胞的侵袭和迁移。我们的研究结果为前列腺癌的治疗提供了理论靶标基础。