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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...

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Autores principales: Han, Xinghua, Wang, Zhanggui, Hu, Bin, Xu, Jianming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
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.
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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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