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Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma
Endostar is a novel artificially-synthesized anti-angiogenesis drug, and has been approved for clinical use. Previous studies have indicated that patients with esophageal cancer could benefit from Endostar combined with chemotherapy or chemoradiotherapy. However, the most advantageous use of this dr...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5686445/ https://www.ncbi.nlm.nih.gov/pubmed/29163691 http://dx.doi.org/10.3892/ol.2017.7017 |
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author | Han, Xinghua Wang, Zhanggui Hu, Bin Xu, Jianming |
author_facet | Han, Xinghua Wang, Zhanggui Hu, Bin Xu, Jianming |
author_sort | Han, Xinghua |
collection | PubMed |
description | Endostar is a novel artificially-synthesized anti-angiogenesis drug, and has been approved for clinical use. Previous studies have indicated that patients with esophageal cancer could benefit from Endostar combined with chemotherapy or chemoradiotherapy. However, the most advantageous use of this drug remains to be elucidated. The role of autophagy in cancer treatment remains controversial. The results of the present study demonstrated that Endostar promotes autophagy activation, which is regulated via phosphorylation inhibition of the downstream signaling molecules of the vascular endothelial growth factor, AKT serine/threonine kinase and mechanistic target of rapamycin signaling pathways. Furthermore, inhibiting autophagy using the pharmacological inhibitor chloroquine facilitated the antiproliferative effect of Endostar and increased the number of apoptotic cells, compared with Endostar monotherapy. Taken together, the results of the present study suggest that autophagy activation induced by Endostar serves a protective role in human esophageal cancer treatment, and that autophagy inhibition promotes the antiproliferative role of Endostar. Therefore, the combination of Endostar with an autophagy inhibitor may be a novel prospective approach to improving the efficacy of Endostar for the treatment of patients with esophageal cancer. |
format | Online Article Text |
id | pubmed-5686445 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-56864452017-11-21 Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma Han, Xinghua Wang, Zhanggui Hu, Bin Xu, Jianming Oncol Lett Articles Endostar is a novel artificially-synthesized anti-angiogenesis drug, and has been approved for clinical use. Previous studies have indicated that patients with esophageal cancer could benefit from Endostar combined with chemotherapy or chemoradiotherapy. However, the most advantageous use of this drug remains to be elucidated. The role of autophagy in cancer treatment remains controversial. The results of the present study demonstrated that Endostar promotes autophagy activation, which is regulated via phosphorylation inhibition of the downstream signaling molecules of the vascular endothelial growth factor, AKT serine/threonine kinase and mechanistic target of rapamycin signaling pathways. Furthermore, inhibiting autophagy using the pharmacological inhibitor chloroquine facilitated the antiproliferative effect of Endostar and increased the number of apoptotic cells, compared with Endostar monotherapy. Taken together, the results of the present study suggest that autophagy activation induced by Endostar serves a protective role in human esophageal cancer treatment, and that autophagy inhibition promotes the antiproliferative role of Endostar. Therefore, the combination of Endostar with an autophagy inhibitor may be a novel prospective approach to improving the efficacy of Endostar for the treatment of patients with esophageal cancer. D.A. Spandidos 2017-12 2017-09-21 /pmc/articles/PMC5686445/ /pubmed/29163691 http://dx.doi.org/10.3892/ol.2017.7017 Text en Copyright: © Han 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 Han, Xinghua Wang, Zhanggui Hu, Bin Xu, Jianming Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title | Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title_full | Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title_fullStr | Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title_full_unstemmed | Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title_short | Autophagy inhibition contributes to Endostar sensitization in esophageal squamous cell carcinoma |
title_sort | autophagy inhibition contributes to endostar sensitization in esophageal squamous cell carcinoma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5686445/ https://www.ncbi.nlm.nih.gov/pubmed/29163691 http://dx.doi.org/10.3892/ol.2017.7017 |
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