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Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells
BACKGROUND: Metastasis is the main cause of lung cancer death. As a seed of metastasis, circulating tumor cells are an important target for metastasis intervention. The traditional Chinese medicine, Jinfukang, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). In...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686466/ https://www.ncbi.nlm.nih.gov/pubmed/31391058 http://dx.doi.org/10.1186/s12906-019-2601-x |
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author | Que, Zujun Zhou, Zhiyi Luo, Bin Dong, Changsheng Jiang, Yi Li, Hegen Tian, Jianhui |
author_facet | Que, Zujun Zhou, Zhiyi Luo, Bin Dong, Changsheng Jiang, Yi Li, Hegen Tian, Jianhui |
author_sort | Que, Zujun |
collection | PubMed |
description | BACKGROUND: Metastasis is the main cause of lung cancer death. As a seed of metastasis, circulating tumor cells are an important target for metastasis intervention. The traditional Chinese medicine, Jinfukang, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). In this study, we investigated the action and underlying mechanisms of Jinfukang against circulating lung tumor cells. METHODS: The cell counting kit-8 (CCK-8), colony formation and cell cycle assays were used to study the cell proliferation ability. Flow cytometry was used to detect the apoptosis and the expression level of ROS and Caspase-3. Comet and TUNEL assays were used to detect DNA damage. DNA damage related pathway protein was detected by western blot. RESULTS: Jinfukang significantly inhibits the proliferation of CTC-TJH-01 cells by inducing G1 phase arrest and inhibits their colony formation in a dose-dependent manner. Moreover, Jinfukang induces apoptosis in CTC-TJH-01 cells through the ROS-mediated ATM/ATR-p53 pathway and DNA damage. CONCLUSIONS: Our findings suggest that Jinfukang may be a potential drug for lung cancer metastasis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12906-019-2601-x) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6686466 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-66864662019-08-12 Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells Que, Zujun Zhou, Zhiyi Luo, Bin Dong, Changsheng Jiang, Yi Li, Hegen Tian, Jianhui BMC Complement Altern Med Research Article BACKGROUND: Metastasis is the main cause of lung cancer death. As a seed of metastasis, circulating tumor cells are an important target for metastasis intervention. The traditional Chinese medicine, Jinfukang, has been clinically available for the treatment of non-small cell lung cancer (NSCLC). In this study, we investigated the action and underlying mechanisms of Jinfukang against circulating lung tumor cells. METHODS: The cell counting kit-8 (CCK-8), colony formation and cell cycle assays were used to study the cell proliferation ability. Flow cytometry was used to detect the apoptosis and the expression level of ROS and Caspase-3. Comet and TUNEL assays were used to detect DNA damage. DNA damage related pathway protein was detected by western blot. RESULTS: Jinfukang significantly inhibits the proliferation of CTC-TJH-01 cells by inducing G1 phase arrest and inhibits their colony formation in a dose-dependent manner. Moreover, Jinfukang induces apoptosis in CTC-TJH-01 cells through the ROS-mediated ATM/ATR-p53 pathway and DNA damage. CONCLUSIONS: Our findings suggest that Jinfukang may be a potential drug for lung cancer metastasis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12906-019-2601-x) contains supplementary material, which is available to authorized users. BioMed Central 2019-08-07 /pmc/articles/PMC6686466/ /pubmed/31391058 http://dx.doi.org/10.1186/s12906-019-2601-x Text en © The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Que, Zujun Zhou, Zhiyi Luo, Bin Dong, Changsheng Jiang, Yi Li, Hegen Tian, Jianhui Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title | Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title_full | Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title_fullStr | Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title_full_unstemmed | Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title_short | Jingfukang induces anti-cancer activity through oxidative stress-mediated DNA damage in circulating human lung cancer cells |
title_sort | jingfukang induces anti-cancer activity through oxidative stress-mediated dna damage in circulating human lung cancer cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686466/ https://www.ncbi.nlm.nih.gov/pubmed/31391058 http://dx.doi.org/10.1186/s12906-019-2601-x |
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