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Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy
High incidence and mortality rates for non‐small‐cell lung cancer (NSCLC) lead to low survival rates. Epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI) are commonly first prescribed for NSCLC patients with EGFR mutations. However, most patients with sensitizing EGFR mutations be...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004076/ https://www.ncbi.nlm.nih.gov/pubmed/31411813 http://dx.doi.org/10.1002/cyto.a.23869 |
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author | Zhang, Jue Sun, Lingling Cui, Jian Wang, Jing Liu, Xiaomin Aung, Thazin Nwe Qu, Zhipeng Chen, Zhuangzhong Adelson, David L. Lin, Lizhu |
author_facet | Zhang, Jue Sun, Lingling Cui, Jian Wang, Jing Liu, Xiaomin Aung, Thazin Nwe Qu, Zhipeng Chen, Zhuangzhong Adelson, David L. Lin, Lizhu |
author_sort | Zhang, Jue |
collection | PubMed |
description | High incidence and mortality rates for non‐small‐cell lung cancer (NSCLC) lead to low survival rates. Epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI) are commonly first prescribed for NSCLC patients with EGFR mutations. However, most patients with sensitizing EGFR mutations become resistant to EGFR‐TKI after 9–13 months treatment. Yiqi Chutan Tang (YQCT) has been prescribed as a treatment to this issue for over 20 years. In this report, high‐performance liquid chromatography (HPLC) analysis, flow cytometry, western blot analysis, and functional annotation analysis were applied to uncover the molecular mechanisms of YQCT. Our results show the application of YQCT reduces gefitinib‐induced drug resistance, induces slight cell cycle arrest, enhances gefitinib‐induced apoptosis, and activates the autophagy. These results indicate that at the molecular level YQCT can reduce drug resistance and improve anti‐cancer effects when associated with gefitinib, which could be a result of enhancement of apoptosis and autophagy in the EGFR‐TKI resistant cells of NSCLC. This research provides a new treatment strategy for patients with EGFR‐TKI resistance in NSCLC. © 2019 The Authors. Cytometry Part A published by Wiley Periodicals, Inc. on behalf of International Society for Advancement of Cytometry. |
format | Online Article Text |
id | pubmed-7004076 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley & Sons, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-70040762020-02-11 Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy Zhang, Jue Sun, Lingling Cui, Jian Wang, Jing Liu, Xiaomin Aung, Thazin Nwe Qu, Zhipeng Chen, Zhuangzhong Adelson, David L. Lin, Lizhu Cytometry A Original Articles High incidence and mortality rates for non‐small‐cell lung cancer (NSCLC) lead to low survival rates. Epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI) are commonly first prescribed for NSCLC patients with EGFR mutations. However, most patients with sensitizing EGFR mutations become resistant to EGFR‐TKI after 9–13 months treatment. Yiqi Chutan Tang (YQCT) has been prescribed as a treatment to this issue for over 20 years. In this report, high‐performance liquid chromatography (HPLC) analysis, flow cytometry, western blot analysis, and functional annotation analysis were applied to uncover the molecular mechanisms of YQCT. Our results show the application of YQCT reduces gefitinib‐induced drug resistance, induces slight cell cycle arrest, enhances gefitinib‐induced apoptosis, and activates the autophagy. These results indicate that at the molecular level YQCT can reduce drug resistance and improve anti‐cancer effects when associated with gefitinib, which could be a result of enhancement of apoptosis and autophagy in the EGFR‐TKI resistant cells of NSCLC. This research provides a new treatment strategy for patients with EGFR‐TKI resistance in NSCLC. © 2019 The Authors. Cytometry Part A published by Wiley Periodicals, Inc. on behalf of International Society for Advancement of Cytometry. John Wiley & Sons, Inc. 2019-08-14 2020-01 /pmc/articles/PMC7004076/ /pubmed/31411813 http://dx.doi.org/10.1002/cyto.a.23869 Text en © 2019 The Authors. Cytometry Part A published by Wiley Periodicals, Inc. on behalf of International Society for Advancement of Cytometry. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles Zhang, Jue Sun, Lingling Cui, Jian Wang, Jing Liu, Xiaomin Aung, Thazin Nwe Qu, Zhipeng Chen, Zhuangzhong Adelson, David L. Lin, Lizhu Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title | Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title_full | Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title_fullStr | Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title_full_unstemmed | Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title_short | Yiqi Chutan Tang Reduces Gefitinib‐Induced Drug Resistance in Non‐Small‐Cell Lung Cancer by Targeting Apoptosis and Autophagy |
title_sort | yiqi chutan tang reduces gefitinib‐induced drug resistance in non‐small‐cell lung cancer by targeting apoptosis and autophagy |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004076/ https://www.ncbi.nlm.nih.gov/pubmed/31411813 http://dx.doi.org/10.1002/cyto.a.23869 |
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