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MicroRNA-4491 enhances cell proliferation and inhibits cell apoptosis in non-small cell lung cancer via targeting TRIM7

MicroRNAs (miRNAs) are involved in the development of non-small cell lung cancer (NSCLC). However, the biological roles of several aberrantly expressed miRNAs have not been explored yet. In the present study, miR-4491 was identified as a novel upregulated miRNA in NSCLC tissues and cell lines. Downr...

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Detalles Bibliográficos
Autores principales: Han, Fei, Chen, Gang, Guo, Yi, Li, Bo, Sun, Yanlong, Qi, Xiangqian, Tian, Hanji, Zhao, Xinfei, Zhang, Hongguang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8200940/
https://www.ncbi.nlm.nih.gov/pubmed/34149902
http://dx.doi.org/10.3892/ol.2021.12852
Descripción
Sumario:MicroRNAs (miRNAs) are involved in the development of non-small cell lung cancer (NSCLC). However, the biological roles of several aberrantly expressed miRNAs have not been explored yet. In the present study, miR-4491 was identified as a novel upregulated miRNA in NSCLC tissues and cell lines. Downregulation of miR-4491 by a miR-4491 inhibitor inhibited the proliferation and triggered the apoptosis of NSCLC cells. Tripartite motif containing 7 (TRIM7), a tumor suppressor gene expressed in NSCLC, was demonstrated in the present study to be directly targeted by miR-4491. This finding was verified by bioinformatics analysis, reverse transcription-quantitative PCR, western blotting and dual luciferase reporter assays. Furthermore, downregulation of miR-4491 inactivated nuclear factor-κB signaling via induction of TRIM7. In addition, TRIM7 silencing attenuated the effect of miR-4491 inhibitor in NSCLC cells. The decreased TRIM7 level in NSCLC tissues was negatively correlated with miR-4491 expression in NSCLC tissues. In conclusion, the findings from this study demonstrated that miR-4491 expression was upregulated in NSCLC tissues and cells and that miR-4491 may promote NSCLC progression via targeting TRIM7.