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Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer

PURPOSE: Recent studies demonstrate the possible antitumor effects of granulocyte-macrophage colony-stimulating factor (GM-CSF); however, the exact mechanism is still unclear. The aim of our study was to analyze the effects of GM-CSF on multiple biological functions of human esophageal cancer (EC) c...

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Autores principales: Zhang, Jingxin, Liu, Qiqi, Qiao, Lili, Hu, Pingping, Deng, Guodong, Liang, Ning, Xie, Jian, Luo, Hui, Zhang, Jiandong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5404808/
https://www.ncbi.nlm.nih.gov/pubmed/28461757
http://dx.doi.org/10.2147/OTT.S133504
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author Zhang, Jingxin
Liu, Qiqi
Qiao, Lili
Hu, Pingping
Deng, Guodong
Liang, Ning
Xie, Jian
Luo, Hui
Zhang, Jiandong
author_facet Zhang, Jingxin
Liu, Qiqi
Qiao, Lili
Hu, Pingping
Deng, Guodong
Liang, Ning
Xie, Jian
Luo, Hui
Zhang, Jiandong
author_sort Zhang, Jingxin
collection PubMed
description PURPOSE: Recent studies demonstrate the possible antitumor effects of granulocyte-macrophage colony-stimulating factor (GM-CSF); however, the exact mechanism is still unclear. The aim of our study was to analyze the effects of GM-CSF on multiple biological functions of human esophageal cancer (EC) cell lines and to explore the potential mechanism of its antitumor effects. MATERIALS AND METHODS: Eca109/9706 human EC cells were examined. Cell proliferation, apoptosis, and migration were analyzed using cell proliferation assay, flow cytometry, and transwell assay, respectively. The expression of signaling molecules were examined by reverse transcription polymerase chain reaction and Western blot. RESULTS: Our results provide experimental evidence that GM-CSF inhibits growth and migration, as well as induction of apoptosis in EC cells. In addition, EC cells stimulated with GM-CSF were more likely to have suppressed epithelial-to-mesenchymal transition (EMT), accompanied by increased E-cadherin and decreased vimentin expression. CONCLUSION: Our data demonstrate that GM-CSF inhibits cancer cell proliferation and migration, as well as induction of apoptosis. Moreover, our findings indicate that GM-CSF may regulate EMT through JAK2-PRMT5 signaling, and thereby exhibit its antitumor effects on EC cells.
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spelling pubmed-54048082017-05-01 Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer Zhang, Jingxin Liu, Qiqi Qiao, Lili Hu, Pingping Deng, Guodong Liang, Ning Xie, Jian Luo, Hui Zhang, Jiandong Onco Targets Ther Original Research PURPOSE: Recent studies demonstrate the possible antitumor effects of granulocyte-macrophage colony-stimulating factor (GM-CSF); however, the exact mechanism is still unclear. The aim of our study was to analyze the effects of GM-CSF on multiple biological functions of human esophageal cancer (EC) cell lines and to explore the potential mechanism of its antitumor effects. MATERIALS AND METHODS: Eca109/9706 human EC cells were examined. Cell proliferation, apoptosis, and migration were analyzed using cell proliferation assay, flow cytometry, and transwell assay, respectively. The expression of signaling molecules were examined by reverse transcription polymerase chain reaction and Western blot. RESULTS: Our results provide experimental evidence that GM-CSF inhibits growth and migration, as well as induction of apoptosis in EC cells. In addition, EC cells stimulated with GM-CSF were more likely to have suppressed epithelial-to-mesenchymal transition (EMT), accompanied by increased E-cadherin and decreased vimentin expression. CONCLUSION: Our data demonstrate that GM-CSF inhibits cancer cell proliferation and migration, as well as induction of apoptosis. Moreover, our findings indicate that GM-CSF may regulate EMT through JAK2-PRMT5 signaling, and thereby exhibit its antitumor effects on EC cells. Dove Medical Press 2017-04-20 /pmc/articles/PMC5404808/ /pubmed/28461757 http://dx.doi.org/10.2147/OTT.S133504 Text en © 2017 Zhang et al. 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.
spellingShingle Original Research
Zhang, Jingxin
Liu, Qiqi
Qiao, Lili
Hu, Pingping
Deng, Guodong
Liang, Ning
Xie, Jian
Luo, Hui
Zhang, Jiandong
Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title_full Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title_fullStr Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title_full_unstemmed Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title_short Novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
title_sort novel role of granulocyte-macrophage colony-stimulating factor: antitumor effects through inhibition of epithelial-to-mesenchymal transition in esophageal cancer
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5404808/
https://www.ncbi.nlm.nih.gov/pubmed/28461757
http://dx.doi.org/10.2147/OTT.S133504
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