NUAK1 knockdown suppresses prostate cancer cell epithelial-mesenchymal transition, migration, and invasion through microRNA-30b-5p

被引:2
|
作者
Guan, Yongjun [1 ]
Shi, Hongbo [1 ]
Xiao, Tianlin [1 ]
机构
[1] Hubei Univ Arts & Sci, Dept Urol, Xiangyang Cent Hosp, Affiliated Hosp, 39 Jingzhou St, Xiangyang 441021, Hubei, Peoples R China
关键词
Prostate cancer; NUAK1; miR-30b-5p; epithelial-mesenchymal transition; migration; invasion; TUMOR-SUPPRESSOR; TARGETING NUAK1; METASTASIS; EXPRESSION; PROGNOSIS; EMT;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Objective: Prostate cancer is one of the most diagnosed malignancies in men worldwide. Novel (nua) kinase family 1 (NUAK1) is a member of adenosine monophosphate (AMP)-related kinase which participates in varying cancers progression. However, the role of NUAK1 in prostate tumorigenesis has not been fully characterized. The aim of this study was to elucidate the potential biological role of NUAK1 in prostate cancer. Methods: Quantitative real-time PCR (qRT-PCR) was performed to determine the expression levels of NUAK1 and microRNA-30b-5p (miRNA-30b-5p) in prostate cancer cell lines and samples. Western blot was conducted to explore the related protein levels of epithelial-mesenchymal transition (EMT) and NUAK1 expression in prostate cancer cells. Trans-well test was used to assay prostate cancer cell migration and invasion. Luciferase assays were employed to probe the interaction between NUAK1 and miR-30b-5p. Results: NUAK1 abundance was enhanced in prostate cancer tissues and cell lines. The knockdown of NUAK1 may inhibit prostate cancer cells EMT, migration and invasion. Luciferase assays suggested NUAK1 was a target gene of miR-30b-5p. Furthermore, miR-30b-5p suppressed EMT, migration, and invasion in prostate cancer cells and introduction of NUAK1 abated the inhibitory effect. Conclusions: Both of NUAK1 and miR-30b-5p were required for prostate cancer progression. NUAK1 interference limited prostate cancer cell EMT, migration and invasion by miRNA-30b-5p modulating, providing a promising therapeutic approach for prostate cancer.
引用
收藏
页码:5694 / 5704
页数:11
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