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miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR
The present study aimed to further explore the molecular mechanisms of miRNA-223 in non-small cell lung cancer (NSCLC). Data prospectively collected from NSCLC patients and volunteers from March 2016 to May 2016 at Tsinghua Changgung Hospital were analyzed. Cell proliferation was measured using MTT...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365711/ https://www.ncbi.nlm.nih.gov/pubmed/30747217 http://dx.doi.org/10.3892/or.2019.6983 |
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author | Ma, Hui-Ping Kong, Wei-Xiang Li, Xiu-Ying Li, Wei Zhang, Yan Wu, Yan |
author_facet | Ma, Hui-Ping Kong, Wei-Xiang Li, Xiu-Ying Li, Wei Zhang, Yan Wu, Yan |
author_sort | Ma, Hui-Ping |
collection | PubMed |
description | The present study aimed to further explore the molecular mechanisms of miRNA-223 in non-small cell lung cancer (NSCLC). Data prospectively collected from NSCLC patients and volunteers from March 2016 to May 2016 at Tsinghua Changgung Hospital were analyzed. Cell proliferation was measured using MTT assay, while cell apoptosis and caspase-3/9 activity were measured using flow cytometry and caspase-3/9 activity kit. Bax, EGFR, PI3K and p-Akt protein were also investigated using western blotting. The results revealed that the serum levels of miRNA-223 in NSCLC patients were downregulated. In an in vitro model, overexpression of miRNA-223 induced apoptosis while reducing cell proliferation. In contrast, downregulation of the expression of miRNA-223 inhibited apoptosis whereas it increased cell proliferation. Meanwhile, overexpression of miRNA-223 suppressed the protein expression of EGFR, PI3K and p-Akt in NSCLC cells. An EGFR inhibitor promoted the anticancer effects of miRNA-223 in NSCLC cells through the EGFR/PI3K/AKT pathway. Meanwhile, a PI3K inhibitor increased the anticancer effects of miRNA-223 in NSCLC cells through the PI3K/AKT pathway. Thus, a new pathway has been identified in the present study, and application of miRNA-223 may induce the apoptosis of NSCLC through the PI3K/AKT pathway by EGFR. |
format | Online Article Text |
id | pubmed-6365711 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63657112019-02-23 miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR Ma, Hui-Ping Kong, Wei-Xiang Li, Xiu-Ying Li, Wei Zhang, Yan Wu, Yan Oncol Rep Articles The present study aimed to further explore the molecular mechanisms of miRNA-223 in non-small cell lung cancer (NSCLC). Data prospectively collected from NSCLC patients and volunteers from March 2016 to May 2016 at Tsinghua Changgung Hospital were analyzed. Cell proliferation was measured using MTT assay, while cell apoptosis and caspase-3/9 activity were measured using flow cytometry and caspase-3/9 activity kit. Bax, EGFR, PI3K and p-Akt protein were also investigated using western blotting. The results revealed that the serum levels of miRNA-223 in NSCLC patients were downregulated. In an in vitro model, overexpression of miRNA-223 induced apoptosis while reducing cell proliferation. In contrast, downregulation of the expression of miRNA-223 inhibited apoptosis whereas it increased cell proliferation. Meanwhile, overexpression of miRNA-223 suppressed the protein expression of EGFR, PI3K and p-Akt in NSCLC cells. An EGFR inhibitor promoted the anticancer effects of miRNA-223 in NSCLC cells through the EGFR/PI3K/AKT pathway. Meanwhile, a PI3K inhibitor increased the anticancer effects of miRNA-223 in NSCLC cells through the PI3K/AKT pathway. Thus, a new pathway has been identified in the present study, and application of miRNA-223 may induce the apoptosis of NSCLC through the PI3K/AKT pathway by EGFR. D.A. Spandidos 2019-03 2019-01-24 /pmc/articles/PMC6365711/ /pubmed/30747217 http://dx.doi.org/10.3892/or.2019.6983 Text en Copyright: © Ma 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 Ma, Hui-Ping Kong, Wei-Xiang Li, Xiu-Ying Li, Wei Zhang, Yan Wu, Yan miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title | miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title_full | miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title_fullStr | miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title_full_unstemmed | miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title_short | miRNA-223 is an anticancer gene in human non-small cell lung cancer through the PI3K/AKT pathway by targeting EGFR |
title_sort | mirna-223 is an anticancer gene in human non-small cell lung cancer through the pi3k/akt pathway by targeting egfr |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365711/ https://www.ncbi.nlm.nih.gov/pubmed/30747217 http://dx.doi.org/10.3892/or.2019.6983 |
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