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LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma
BACKGROUND: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin res...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7519870/ https://www.ncbi.nlm.nih.gov/pubmed/33061421 http://dx.doi.org/10.2147/OTT.S244879 |
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author | Wang, Junbin Gao, Jin Chen, Qinnan Zou, Weiyan Yang, Fen Wei, Chenchen Wang, Zhaoxia |
author_facet | Wang, Junbin Gao, Jin Chen, Qinnan Zou, Weiyan Yang, Fen Wei, Chenchen Wang, Zhaoxia |
author_sort | Wang, Junbin |
collection | PubMed |
description | BACKGROUND: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). MATERIALS AND METHODS: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. RESULTS: MTT assay measured the IC(50) values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82-fold increase in Vimentin expression in A549 cells. CONCLUSION: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin. |
format | Online Article Text |
id | pubmed-7519870 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-75198702020-10-14 LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma Wang, Junbin Gao, Jin Chen, Qinnan Zou, Weiyan Yang, Fen Wei, Chenchen Wang, Zhaoxia Onco Targets Ther Original Research BACKGROUND: Long non-coding RNAs (lncRNAs) have been found to contribute to cisplatin resistance in several cancers; however, the role of lncRNA LINC01116 in cisplatin resistance remains unknown in non-small-cell lung cancer. This study aimed to examine the contribution of LINC01116 to cisplatin resistance in lung adenocarcinoma (LAD). MATERIALS AND METHODS: Cisplatin-resistant A549/DDP cells were generated by treatment with cisplatin by dose escalation. LINC01116 expression was compared between A549 and A549/DDP cells, and between cisplatin-resistant and non-resistant LAD specimens. The cell viability, colony formation, proliferation, migration and invasion were measured using MTT and Transwell assays, and cell apoptosis and cell cycle were detected using flow cytometry. The expression of E-cadherin and Vimentin was quantified. LAD xenografts were modeled in nude mice to investigate the role of LINC01116 on the resistance of LAD to cisplatin. RESULTS: MTT assay measured the IC(50) values of 13.49 ± 1.62 and 3.52 ± 1.33 μg/mL for A549/DDP and A549 cells, respectively. LINC01116 was overexpressed in cisplatin-resistant LAD specimens and A549/DDP cells (P < 0.05). Knockdown of LINC01116 inhibited cell viability, proliferation, migration and invasion, promoted apoptosis and enhanced the sensitivity to cisplatin in A549/DDP cells, while LINC01116 overexpression promoted cell viability, proliferation, migration and invasion, inhibited apoptosis and reduced the sensitivity to cisplatin in A549 cells. LINC01116 knockdown resulted in a 2.1-fold increase in E-cadherin expression and a 56% reduction in Vimentin expression in A549/DDP cells, and LINC01116 overexpression resulted in a 45% reduction in E-cadherin expression and a 1.82-fold increase in Vimentin expression in A549 cells. CONCLUSION: Dysregulation of lncRNA LINC01116 expression results in resistance of LAD to cisplatin via the EMT process. Our findings support the oncogenic role of LINC01116 to promote the development of cisplatin resistance in LAD, and LINC01116 may be a novel predictor of poor response to cisplatin. Dove 2020-09-22 /pmc/articles/PMC7519870/ /pubmed/33061421 http://dx.doi.org/10.2147/OTT.S244879 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wang, Junbin Gao, Jin Chen, Qinnan Zou, Weiyan Yang, Fen Wei, Chenchen Wang, Zhaoxia LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title | LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title_full | LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title_fullStr | LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title_full_unstemmed | LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title_short | LncRNA LINC01116 Contributes to Cisplatin Resistance in Lung Adenocarcinoma |
title_sort | lncrna linc01116 contributes to cisplatin resistance in lung adenocarcinoma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7519870/ https://www.ncbi.nlm.nih.gov/pubmed/33061421 http://dx.doi.org/10.2147/OTT.S244879 |
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