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，因为早期诊断困难，目前尚无有效治疗方法。据报道，miRNA-217-5p是前列腺癌过程中的调节因子。本研究旨在探讨miRNA-217-5p如何影响前列腺癌的侵袭和迁移。使用荧光素酶测定来阐明靶基因 Clusterin (CLU) 是否直接与 miR-217-5p 相互作用。通过将各自的 siRNA 转染至 DU145 细胞中来敲低 miR-217-5p 和 CLU。采用Western blotting检测上皮间质转化（EMT）相关蛋白的表达水平。通过伤口愈合实验检测DU145细胞的侵袭和迁移。结果表明miR-217-5p直接与其靶基因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株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，进一步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。并进一步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。并进一步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。