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
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
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