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Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality in the United States. Chemotherapy prolongs survival rates among patients with advanced disease, however, this is at the cost of clinically significant adverse effects. Matrine is an active component of traditiona...

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Autores principales: An, Qi, Han, Chao, Zhou, Yubing, Li, Feng, Li, Duolu, Zhang, Xiaojian, Yu, Zujiang, Duan, Zhenfeng, Kan, Quancheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5101874/
https://www.ncbi.nlm.nih.gov/pubmed/27665734
http://dx.doi.org/10.3892/mmr.2016.5753
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author An, Qi
Han, Chao
Zhou, Yubing
Li, Feng
Li, Duolu
Zhang, Xiaojian
Yu, Zujiang
Duan, Zhenfeng
Kan, Quancheng
author_facet An, Qi
Han, Chao
Zhou, Yubing
Li, Feng
Li, Duolu
Zhang, Xiaojian
Yu, Zujiang
Duan, Zhenfeng
Kan, Quancheng
author_sort An, Qi
collection PubMed
description Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality in the United States. Chemotherapy prolongs survival rates among patients with advanced disease, however, this is at the cost of clinically significant adverse effects. Matrine is an active component of traditional Chinese medicine and is a promising alternative drug for the treatment of NSCLC. In the present study, the therapeutic effects and the underlying molecular mechanisms of matrine on the A549 NSCLC cell line were investigated. A high concentration of matrine (1.0 mg/ml) significantly (P<0.05) inhibited cell proliferation, by 52.68±3.32%, under which cell shrinkage and disruption were observed. Flow cytometric analysis showed that the proportion of G1/G0 cells was significantly increased, whereas the proportions of S and G2/M cells were significantly decreased (P<0.05) following treatment with matrine for 48 h. These results indicated that cell arrest was induced by matrine. Upregulation of the expression of microRNA (miR)-126, followed by downregulation of the expression of its target gene, vascular endothelial growth factor, were detected following treatment with a low concentration of matrine (0.2 mg/ml) using reverse transcription-quantitative polymerase chain reaction analysis, immunohistochemistry and western blot analysis. In conclusion, matrine induced cell cycle arrest and apoptosis, and recovered the expression of miR-126 in the A549 NSCLC cell line.
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spelling pubmed-51018742016-11-22 Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line An, Qi Han, Chao Zhou, Yubing Li, Feng Li, Duolu Zhang, Xiaojian Yu, Zujiang Duan, Zhenfeng Kan, Quancheng Mol Med Rep Articles Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated mortality in the United States. Chemotherapy prolongs survival rates among patients with advanced disease, however, this is at the cost of clinically significant adverse effects. Matrine is an active component of traditional Chinese medicine and is a promising alternative drug for the treatment of NSCLC. In the present study, the therapeutic effects and the underlying molecular mechanisms of matrine on the A549 NSCLC cell line were investigated. A high concentration of matrine (1.0 mg/ml) significantly (P<0.05) inhibited cell proliferation, by 52.68±3.32%, under which cell shrinkage and disruption were observed. Flow cytometric analysis showed that the proportion of G1/G0 cells was significantly increased, whereas the proportions of S and G2/M cells were significantly decreased (P<0.05) following treatment with matrine for 48 h. These results indicated that cell arrest was induced by matrine. Upregulation of the expression of microRNA (miR)-126, followed by downregulation of the expression of its target gene, vascular endothelial growth factor, were detected following treatment with a low concentration of matrine (0.2 mg/ml) using reverse transcription-quantitative polymerase chain reaction analysis, immunohistochemistry and western blot analysis. In conclusion, matrine induced cell cycle arrest and apoptosis, and recovered the expression of miR-126 in the A549 NSCLC cell line. D.A. Spandidos 2016-11 2016-09-20 /pmc/articles/PMC5101874/ /pubmed/27665734 http://dx.doi.org/10.3892/mmr.2016.5753 Text en Copyright: © An 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
An, Qi
Han, Chao
Zhou, Yubing
Li, Feng
Li, Duolu
Zhang, Xiaojian
Yu, Zujiang
Duan, Zhenfeng
Kan, Quancheng
Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title_full Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title_fullStr Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title_full_unstemmed Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title_short Matrine induces cell cycle arrest and apoptosis with recovery of the expression of miR-126 in the A549 non-small cell lung cancer cell line
title_sort matrine induces cell cycle arrest and apoptosis with recovery of the expression of mir-126 in the a549 non-small cell lung cancer cell line
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5101874/
https://www.ncbi.nlm.nih.gov/pubmed/27665734
http://dx.doi.org/10.3892/mmr.2016.5753
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