RETRACTED: miR-217-5p Inhibits Invasion and Metastasis of Prostate Cancer by Targeting Clusterin (Retracted article. See JUN, 2023)

被引:16
|
作者
Zhao, Wanli [1 ,2 ]
Wang, Xiuli [3 ]
Jiang, Yuqing [1 ]
Jia, Xiaopeng [1 ]
Guo, Yuexian [1 ]
机构
[1] Hebei Med Univ, Hosp 3, Dept Urol, 139 Ziqiang Rd, Shijiazhuang 050001, Hebei, Peoples R China
[2] Cangzhou Cent Hosp, Dept Urol 2, 16,Xinhua West Rd, Cangzhou 061001, Hebei, Peoples R China
[3] Hebei Med Univ, Hosp 3, Dept Anesthesiol, 139,Ziqiang Rd, Shijiazhuang 050001, Hebei, Peoples R China
关键词
LONG NONCODING RNA; HEPATOCELLULAR-CARCINOMA; PREDNISONE; EXPRESSION; DOCETAXEL; GROWTH; CELLS; GENE;
D O I
10.1007/s00335-021-09874-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:371 / 380
页数:10
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