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An epithelial-to-mesenchymal transition-inducing potential of granulocyte macrophage colony-stimulating factor in colon cancer.

An epithelial-to-mesenchymal transition-inducing potential of granulocyte macrophage colony-stimulating factor in colon cancer.
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Chen Y, Zhao Z, Chen Y, Lv Z, Ding X, Wang R, Xiao H, Hou C, Shen B, Feng J, Guo R, Li Y, Peng H, Han G, Chen G,


Chen Y, Zhao Z, Chen Y, Lv Z, Ding X, Wang R, Xiao H, Hou C, Shen B, Feng J, Guo R, Li Y, Peng H, Han G, Chen G, (click to view)

Chen Y, Zhao Z, Chen Y, Lv Z, Ding X, Wang R, Xiao H, Hou C, Shen B, Feng J, Guo R, Li Y, Peng H, Han G, Chen G,

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Scientific reports 2017 08 157(1) 8265 doi 10.1038/s41598-017-08047-1
Abstract

Growing evidence shows that granulocyte macrophage colony-stimulating factor (GM-CSF) has progression-promoting potentials in certain solid tumors, which is largely attributed to the immunomodulatory function of this cytokine in tumor niches. However, little is known about the effect of GM-CSF on cancer cells. Herein, we show that chronic exposure of colon cancer cells to GM-CSF, which harbor its receptor, leads to occurrence of epithelial to mesenchymal transition (EMT), in time and dose-dependent manners. These GM-CSF-educated cancer cells exhibit enhanced ability of motility in vitro and in vivo. Furthermore, GM-CSF stimulation renders colon cancer cells more resistant to cytotoxic agents. Mechanistic investigation reveals that MAPK/ERK signaling and EMT-inducing transcription factor ZEB1 are critical to mediate these effects of GM-CSF. In specimen of CRC patients, high-level expression of GM-CSF positively correlates with local metastases in lymph nodes. Moreover, the co-expression of GM-CSF and its receptors as well as phosphorylated ERK1/2 are observed. Thus, our study for the first time identifies a progression-promoting function of GM-CSF in colon cancer by inducing EMT.

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