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MicroRNA-372 functions as a tumor suppressor in cell invasion, migration and epithelial-mesenchymal transition by targeting ATAD2 in renal cell carcinoma

In recent years, renal cell carcinoma (RCC) has exhibited an increasing incidence and mortality rate worldwide. Accumulating evidence has identified that microRNAs (miRNAs) function as negative or positive regulators of many malignant tumors; however, the roles of miR-372 in RCC remain unclear. The...

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Detalles Bibliográficos
Autores principales: Ji, Shiqi, Su, Xiaolin, Zhang, Haijian, Han, Zhixing, Zhao, Yuqian, Liu, Qingjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6350190/
https://www.ncbi.nlm.nih.gov/pubmed/30719113
http://dx.doi.org/10.3892/ol.2018.9871
Descripción
Sumario:In recent years, renal cell carcinoma (RCC) has exhibited an increasing incidence and mortality rate worldwide. Accumulating evidence has identified that microRNAs (miRNAs) function as negative or positive regulators of many malignant tumors; however, the roles of miR-372 in RCC remain unclear. The focus of the present study was the functions of miR-372 in RCC metastasis and EMT. Data revealed that miR-372 expression levels were significantly downregulated in RCC tissue samples and cells. Moreover, the decreased expression levels were strongly associated with the poor survival rates and adverse clinical characteristics of RCC patients. Accordingly, miR-372 overexpression markedly inhibited RCC cell invasion, migration and EMT. In terms of the potential mechanisms, ATAD2, the expression of which was inversely correlated with miR-372 expression in RCC, was identified as a direct functional target of miR-372. Notably, ATAD2 silence exerted suppressive functions in RCC cells, being similar to the effects of miR-372 overexpression. In conclusion, findings of this study indicate that miR-372 repressed RCC EMT and metastasis via targeting ATAD2, suggesting that the miR-372/ATAD2 axis may be therapeutic biomarkers for RCC.