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MicroRNA-16-1 Inhibits Tumor Cell Proliferation and Induces Apoptosis in A549 Non-Small Cell Lung Carcinoma Cells
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Plenty of microRNAs (miRs), except miR-16-1, have been reported to be associated with the initiation and progression of NSCLC. This study was aimed to explore the impacts of miR-16-1 on NSCLC cells. Human NSCLC cell line A549...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cognizant Communication Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7838694/ https://www.ncbi.nlm.nih.gov/pubmed/27712591 http://dx.doi.org/10.3727/096504016X14685034103194 |
Sumario: | Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Plenty of microRNAs (miRs), except miR-16-1, have been reported to be associated with the initiation and progression of NSCLC. This study was aimed to explore the impacts of miR-16-1 on NSCLC cells. Human NSCLC cell line A549 was used, and the expression of miR-16-1 was up- or downregulated by transfecting with miR-16-1 mimics or inhibitors. Afterward, cell proliferation and apoptosis were detected using MTT assay, BrdU assay, and Annexin V/FITC Apoptosis Detection Kit. The expression changes of proliferation- and apoptosis-related factors were measured by Western blot. Results showed that miR-16-1 overexpression significantly inhibited cell proliferation and induced apoptosis when compared with the control group. Besides, miR-16-1 overexpression significantly upregulated the protein expressions of p27, Bax, procaspase 3, and cleaved caspase 3, whereas it downregulated Bcl-2. Conversely, miR-16-1 suppression affected NSCLC cell proliferation and apoptosis, and these protein expressions resulted in completely opposite impacts. In conclusion, miR-16-1 overexpression could inhibit cell proliferation and induce apoptosis via regulating the expression of p27, Bcl-2, Bax, and caspase 3 in NSCLC cells. |
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