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Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo
Background: Non-small-cell lung cancer (NSCLC) was known as the most malignant tumor. Paclitaxel (PTX) is the effective drug used for the treatment of NSCLC; however, it also exhibits severe side effects. Emodin could induce apoptosis of NSCLC cells and serve as a potential cancer therapeutic agent....
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489594/ https://www.ncbi.nlm.nih.gov/pubmed/31114158 http://dx.doi.org/10.2147/DDDT.S196319 |
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author | Chen, Shuifang Zhang, Zeying Zhang, Jianli |
author_facet | Chen, Shuifang Zhang, Zeying Zhang, Jianli |
author_sort | Chen, Shuifang |
collection | PubMed |
description | Background: Non-small-cell lung cancer (NSCLC) was known as the most malignant tumor. Paclitaxel (PTX) is the effective drug used for the treatment of NSCLC; however, it also exhibits severe side effects. Emodin could induce apoptosis of NSCLC cells and serve as a potential cancer therapeutic agent. However, the effects of combination of emodin with PTX on NSCLC remain unclear. Thus, this study aimed to investigate the effects of emodin in combination with PTX on A549 cells. Materials and methods: The effects of combination treatment on the proliferation, apoptosis and invasion of NSCLC cells were evaluated by CCK-8, flow cytometric and TUNEL assays, respectively. In addition, Western blotting was used to detect the expressions of Bax, Bcl-2, active caspase 3, p-Akt and ERK in cells. Results: Combination of emodin with PTX synergistically inhibited the proliferation of A549 cells in vitro. In addition, we found that emodin significantly enhanced PTX-induced apoptosis in A549 cells via increasing the expressions of Bax and active caspase 3 and decreasing the levels of Bcl-2, p-Akt and p-ERK. Moreover, emodin markedly enhanced antitumor effect of PTX on A549 xenograft without significant side effects in vivo. Conclusion: Our findings indicated that emodin could significantly enhance antitumor effect of PTX in vitro and in vivo. Therefore, the combination of emodin with PTX may serve as a potential strategy for the treatment of patients with NSCLC. |
format | Online Article Text |
id | pubmed-6489594 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-64895942019-05-21 Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo Chen, Shuifang Zhang, Zeying Zhang, Jianli Drug Des Devel Ther Original Research Background: Non-small-cell lung cancer (NSCLC) was known as the most malignant tumor. Paclitaxel (PTX) is the effective drug used for the treatment of NSCLC; however, it also exhibits severe side effects. Emodin could induce apoptosis of NSCLC cells and serve as a potential cancer therapeutic agent. However, the effects of combination of emodin with PTX on NSCLC remain unclear. Thus, this study aimed to investigate the effects of emodin in combination with PTX on A549 cells. Materials and methods: The effects of combination treatment on the proliferation, apoptosis and invasion of NSCLC cells were evaluated by CCK-8, flow cytometric and TUNEL assays, respectively. In addition, Western blotting was used to detect the expressions of Bax, Bcl-2, active caspase 3, p-Akt and ERK in cells. Results: Combination of emodin with PTX synergistically inhibited the proliferation of A549 cells in vitro. In addition, we found that emodin significantly enhanced PTX-induced apoptosis in A549 cells via increasing the expressions of Bax and active caspase 3 and decreasing the levels of Bcl-2, p-Akt and p-ERK. Moreover, emodin markedly enhanced antitumor effect of PTX on A549 xenograft without significant side effects in vivo. Conclusion: Our findings indicated that emodin could significantly enhance antitumor effect of PTX in vitro and in vivo. Therefore, the combination of emodin with PTX may serve as a potential strategy for the treatment of patients with NSCLC. Dove 2019-04-10 /pmc/articles/PMC6489594/ /pubmed/31114158 http://dx.doi.org/10.2147/DDDT.S196319 Text en © 2019 Chen 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 Chen, Shuifang Zhang, Zeying Zhang, Jianli Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title | Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title_full | Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title_fullStr | Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title_full_unstemmed | Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title_short | Emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
title_sort | emodin enhances antitumor effect of paclitaxel on human non-small-cell lung cancer cells in vitro and in vivo |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6489594/ https://www.ncbi.nlm.nih.gov/pubmed/31114158 http://dx.doi.org/10.2147/DDDT.S196319 |
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