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Induction of microRNA-let-7a inhibits lung adenocarcinoma cell growth by regulating cyclin D1

Lung cancer is the most common cause of cancer-associated mortality. MicroRNAs (miRNAs), as oncogenes or tumor suppressor genes, serve crucial roles not only in tumorigenesis, but also in tumor invasion and metastasis. Although miRNA-let-7a (let-7a) has been reported to suppress cell growth in multi...

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Detalles Bibliográficos
Autores principales: Zhao, Wei, Hu, Jin-Xia, Hao, Rui-Min, Zhang, Qian, Guo, Jun-Qi, Li, You-Jie, Xie, Ning, Liu, Lu-Ying, Wang, Ping-Yu, Zhang, Can, Xie, Shu-Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6111629/
https://www.ncbi.nlm.nih.gov/pubmed/30066899
http://dx.doi.org/10.3892/or.2018.6593
Descripción
Sumario:Lung cancer is the most common cause of cancer-associated mortality. MicroRNAs (miRNAs), as oncogenes or tumor suppressor genes, serve crucial roles not only in tumorigenesis, but also in tumor invasion and metastasis. Although miRNA-let-7a (let-7a) has been reported to suppress cell growth in multiple cancer types, the biological mechanisms of let-7a in lung adenocarcinoma are yet to be fully elucidated. In the present study, the molecular roles of let-7a in lung adenocarcinoma were investigated by detecting its expression in lung adenocarcinoma tissues and exploring its roles in the regulation of lung cancer cell proliferation. Let-7a expression was identified to be downregulated in lung adenocarcinoma tissues compared with normal tissues. Overexpression of let-7a effectively suppressed cancer cell proliferation, migration and invasion in H1299 and A549 cells. Let-7a also induced cell apoptosis and cell cycle arrest. Furthermore, let-7a significantly inhibited cell growth by directly regulating cyclin D1 signals. This novel regulatory mechanism of let-7a in lung adenocarcinoma provides possible avenues for future targeted therapies of lung cancer.