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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...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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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 |
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. |
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