Back to Journals » OncoTargets and Therapy » Volume 10

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

Authors Zhang J, Liu Q, Qiao L, Hu P, Deng G, Liang N, Xie J, Luo H, Zhang J

Received 30 January 2017

Accepted for publication 17 March 2017

Published 20 April 2017 Volume 2017:10 Pages 2227—2237

DOI https://doi.org/10.2147/OTT.S133504

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Narasimha Reddy Parine

Peer reviewer comments 2

Editor who approved publication: Dr William Cho

Jingxin Zhang,1,* Qiqi Liu,2,* Lili Qiao,3 Pingping Hu,2 Guodong Deng,2 Ning Liang,2 Jian Xie,2 Hui Luo,4 Jiandong Zhang2

1Division of Oncology, Department of Graduate, Weifang Medical College, Weifang, 2Department of Radiation Oncology, Qianfoshan Hospital Affiliated to Shandong University, Shandong University, 3Department of Oncology, The Fifth Peoples’ Hospital of Jinan, Jinan, 4Department of Radiation Oncology, Henan Cancer Hospital Affiliated to Zhengzhou University, Zhengzhou University, Zhengzhou, Henan, People’s Republic of China

*These authors contributed equally to this work

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.

Keywords: granulocyte-macrophage colony-stimulating factor, cancer, antitumor, epithelial-to-mesenchymal transition, esophageal cancer

Creative Commons License 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. 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.

Download Article [PDF]  View Full Text [HTML][Machine readable]

 

Other article by this author:

Soluble cytotoxic T-lymphocyte antigen 4: a favorable predictor in malignant tumors after therapy

Liu Q, Hu P, Deng G, Zhang J, Liang N, Xie J, Qiao L, Luo H, Zhang J

OncoTargets and Therapy 2017, 10:2147-2154

Published Date: 12 April 2017