miR-217-5p Inhibits Invasion and Metastasis of Prostate Cancer by Targeting Clusterin
| Autor: | Yu-Qing Jiang, Yue-Xian Guo, Wanli Zhao, Xiaopeng Jia, Xiuli Wang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
Epithelial-Mesenchymal Transition Cell Biology Metastasis 03 medical and health sciences Prostate cancer 0302 clinical medicine DU145 Genetics medicine Humans Luciferase Neoplasm Invasiveness Neoplasm Metastasis 030304 developmental biology 0303 health sciences Clusterin Prostatic Neoplasms Transfection medicine.disease Blot MicroRNAs medicine.anatomical_structure 030220 oncology & carcinogenesis Cancer research biology.protein |
| Zdroj: | Mammalian genome : official journal of the International Mammalian Genome Society. 32(5) |
| ISSN: | 1432-1777 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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