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miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer

Non-small-cell lung cancer (NSCLC) accounts for 80% of lung cancer cases, and is the leading cause of cancer-associated mortality worldwide. The present study aimed to investigate the roles of microRNA (miR)-654-3p in NSCLC. The expression levels of miR-654-3p and its target ras protein activator li...

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Detalles Bibliográficos
Autores principales: Xiong, Jie, Xing, Shigang, Dong, Zheng, Niu, Lei, Xu, Qinghua, Li, Yusheng, Liu, Pingyi, Yang, Peixia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7751472/
https://www.ncbi.nlm.nih.gov/pubmed/33300072
http://dx.doi.org/10.3892/mmr.2020.11763
Descripción
Sumario:Non-small-cell lung cancer (NSCLC) accounts for 80% of lung cancer cases, and is the leading cause of cancer-associated mortality worldwide. The present study aimed to investigate the roles of microRNA (miR)-654-3p in NSCLC. The expression levels of miR-654-3p and its target ras protein activator like 2 (RASAL2) mRNA were determined by reverse transcription-quantitative polymerase chain reaction; protein expression was analyzed by western blotting. Plasmids expressing miR-654-3p mimics were constructed and transfected into A549 cells. In addition, the viability and apoptotic rate of cells were analyzed by an MTT assay and flow cytometry, respectively. A luciferase reporter assay was performed to verify whether RASAL2 is a target of miR-654-3p. Downregulated miR-654-3p and upregulated RASAL2 expression were observed in tumor tissues and cells. Cell viability was suppressed and the apoptotic rate was increased in the miR-654-3p mimics-transfected cells compared with the control. Luciferase activity was decreased in the RASAL2-3′ untranslated region-wild type group treated with miR-654-3p mimics. Furthermore, the present study revealed that overexpression of miR-654-3p could suppress the viability and induce the apoptosis of cells by targeting RASAL2 in NSCLC. The present findings may contribute to developments in the treatment of NSCLC.