Por favor, use este identificador para citar o enlazar este ítem: DOI: 10.14670/HH-11-772

Título: The suppressive effects of miR-1180-5p on the proliferation and tumorigenicity of bladder cancer cells
Fecha de publicación: 2017
Editorial: Universidad de Murcia. Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and Histopathology, Vol.32, nº1, (2017)
ISSN: 1699-5848
0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: miR-1180-5p
Proliferation
Bladder cancer
Tumorigenicity
Resumen: In our previous research, we have reported that a candidate microRNA (miR-1180-5p) has the capacity to induce overexpression of tumor suppressor gene p21 and inhibit the growth of human bladder cancer (BCa) cell lines in vitro. However, the exact mechanism as to how miR-1180-5p suppresses BCa cell proliferation remains unknown, and the inhibitory effect of miR-1180-5p in vivo also need to be investigated. In the present study, we found that the expression level of miR-1180-5p was lower in BCa cells than in normal human urothelial cells. Furthermore, we found that overexpression of p21, activated by miR-1180-5p, interfered with cell cycle progress by inhibiting the cell cycle related proteins (CDK4, CDK6, Cyclin D1 and Cyclin A2), and thereby suppressed BCa cell proliferation. In addition, miR-1180-5p also suppressed the tumor growth in vivo significantly. Taken together, our study provides evidence that up-regulation of p21 is mainly responsible for the suppressive effect of miR1180-5p on BCa cells and miR-1180-5p can significantly inhibit tumorigenicity in vivo.
Autor/es principal/es: Ge, Qiangqiang
Wang, Chenghe
Chen, Zhong
Li, Fan
Hu, Jia
Ye, Zhangqun
URI: http://hdl.handle.net/10201/116704
DOI: DOI: 10.14670/HH-11-772
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 10
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Aparece en las colecciones:Vol.32, nº1 (2017)

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