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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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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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 |
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author | Xiong, Jie Xing, Shigang Dong, Zheng Niu, Lei Xu, Qinghua Li, Yusheng Liu, Pingyi Yang, Peixia |
author_facet | Xiong, Jie Xing, Shigang Dong, Zheng Niu, Lei Xu, Qinghua Li, Yusheng Liu, Pingyi Yang, Peixia |
author_sort | Xiong, Jie |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7751472 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-77514722020-12-28 miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer Xiong, Jie Xing, Shigang Dong, Zheng Niu, Lei Xu, Qinghua Li, Yusheng Liu, Pingyi Yang, Peixia Mol Med Rep Articles 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. D.A. Spandidos 2021-02 2020-12-08 /pmc/articles/PMC7751472/ /pubmed/33300072 http://dx.doi.org/10.3892/mmr.2020.11763 Text en Copyright: © Xiong et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Xiong, Jie Xing, Shigang Dong, Zheng Niu, Lei Xu, Qinghua Li, Yusheng Liu, Pingyi Yang, Peixia miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title | miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title_full | miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title_fullStr | miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title_full_unstemmed | miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title_short | miR-654-3p suppresses cell viability and promotes apoptosis by targeting RASAL2 in non-small-cell lung cancer |
title_sort | mir-654-3p suppresses cell viability and promotes apoptosis by targeting rasal2 in non-small-cell lung cancer |
topic | Articles |
url | 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 |
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