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lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling
INTRODUCTION: LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC. METHODS: A total of 62 NSCLC pat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260488/ https://www.ncbi.nlm.nih.gov/pubmed/32547220 http://dx.doi.org/10.2147/CMAR.S246422 |
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author | Xiang, Chen Zhang, Yuanli Zhang, Yajing Liu, Ci Hou, Yuehong Zhang, Yan |
author_facet | Xiang, Chen Zhang, Yuanli Zhang, Yajing Liu, Ci Hou, Yuehong Zhang, Yan |
author_sort | Xiang, Chen |
collection | PubMed |
description | INTRODUCTION: LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC. METHODS: A total of 62 NSCLC patients were included to collect paired cancer and non-tumor tissues. RT-qPCR was performed to measure levels of LEF1-AS1 and miR-221 expression. Transient transfections were performed to explore the interactions between LEF1-AS1, miR-221 and PTEN. Cell proliferation and apoptosis were analyzed by cell proliferation assay and cell apoptosis assay, respectively. RESULTS: We found that LEF1-AS1 was upregulated in NSCLC patients. In addition, expression of LEF1-AS1 was negatively correlated with the expression of PTEN but positively correlated with the expression of miR-221 in NSCLC tissue samples. In NSCLC cells, overexpression of LEF1-AS1 led to downregulated expression of PTEN but upregulated expression of miR-221, which can directly target PTEN. Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. PTEN played an opposite role and reduced the effects of overexpressing LEF1-AS1 and miR-221. CONCLUSION: LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling. |
format | Online Article Text |
id | pubmed-7260488 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-72604882020-06-15 lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling Xiang, Chen Zhang, Yuanli Zhang, Yajing Liu, Ci Hou, Yuehong Zhang, Yan Cancer Manag Res Original Research INTRODUCTION: LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC. METHODS: A total of 62 NSCLC patients were included to collect paired cancer and non-tumor tissues. RT-qPCR was performed to measure levels of LEF1-AS1 and miR-221 expression. Transient transfections were performed to explore the interactions between LEF1-AS1, miR-221 and PTEN. Cell proliferation and apoptosis were analyzed by cell proliferation assay and cell apoptosis assay, respectively. RESULTS: We found that LEF1-AS1 was upregulated in NSCLC patients. In addition, expression of LEF1-AS1 was negatively correlated with the expression of PTEN but positively correlated with the expression of miR-221 in NSCLC tissue samples. In NSCLC cells, overexpression of LEF1-AS1 led to downregulated expression of PTEN but upregulated expression of miR-221, which can directly target PTEN. Overexpression of LEF1-AS1 and miR-221 promoted cancer cell proliferation and inhibited apoptosis. PTEN played an opposite role and reduced the effects of overexpressing LEF1-AS1 and miR-221. CONCLUSION: LEF1-AS1 may promote the proliferation and induce apoptosis of NSCLC cells by regulating miR-221/PTEN signaling. Dove 2020-05-25 /pmc/articles/PMC7260488/ /pubmed/32547220 http://dx.doi.org/10.2147/CMAR.S246422 Text en © 2020 Xiang 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 Xiang, Chen Zhang, Yuanli Zhang, Yajing Liu, Ci Hou, Yuehong Zhang, Yan lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title | lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title_full | lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title_fullStr | lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title_full_unstemmed | lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title_short | lncRNA LEF1-AS1 Promotes Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Regulating miR-221/PTEN Signaling |
title_sort | lncrna lef1-as1 promotes proliferation and induces apoptosis of non-small-cell lung cancer cells by regulating mir-221/pten signaling |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260488/ https://www.ncbi.nlm.nih.gov/pubmed/32547220 http://dx.doi.org/10.2147/CMAR.S246422 |
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