MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK

被引:35
作者
Cheng, Yidong [1 ]
Zhang, Xiaolei [1 ]
Li, Peng [1 ]
Yang, Chengdi [1 ]
Tang, Jinyuan [1 ]
Deng, Xiaheng [1 ]
Yang, Xiao [1 ]
Tao, Jun [1 ]
Lu, Qiang [1 ]
Li, Pengchao [1 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Urol, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
miR-200c; bladder cancer; migration; invasion; RECK; DOWN-REGULATION; UROTHELIAL CARCINOMA; TUMOR-METASTASIS; EXPRESSION; MICRORNAS; PROLIFERATION; INHIBITION; BMI-1;
D O I
10.2147/OTT.S101067
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Background: Increasing evidence suggests that the dysregulation of certain microRNAs plays an important role in tumorigenesis and metastasis. MiR-200c exhibits a disordered expression in many tumors and presents dual roles in bladder cancer (BC). Therefore, the definite role of miR-200c in BC needs to be investigated further. Materials and methods: Quantitative reverse transcription polymerase chain reaction was used to assess miR-200c expression. Cell invasion and migration were evaluated using wound healing and transwell assays. The luciferase reporter assay was used to identify the direct target of miR-200c. The expression of reversion-inducing cysteine-rich protein with kazal motifs (RECK) in BC tissues and adjacent nontumor tissues, as well as in BC cell lines, was detected through quantitative reverse transcription polymerase chain reaction, Western blot assay, and immunohistochemistry. Results: The miR-200c expression was significantly upregulated in the BC tissues compared with the adjacent nontumor tissues. The downregulation of miR-200c significantly inhibited cell migration and invasion in the BC cell lines. The luciferase reporter assay showed that RECK was a direct target of miR-200c. The knockdown of RECK in the BC cell lines treated with anti-miR-200c elevated the previously attenuated cell migration and invasion. Conclusion: Our findings indicated that miR-200c functions as oncogenes in BC and may provide a novel therapeutic strategy for the treatment of BC.
引用
收藏
页码:5091 / 5099
页数:9
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