Volume 7 Issue 2
Feb.  2016
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Wenbin Li, Xinghua Zhang, Yongkang Chen, Yibin Xie, Jiancheng Liu, Qiang Feng, Yi Wang, Wei Yuan, Jie Ma. G-CSF is a key modulator of MDSC and could be a potential therapeutic target in colitisassociated colorectal cancers[J]. Protein&Cell, 2016, 7(2): 130-140. doi: 10.1007/s13238-015-0237-2
Citation: Wenbin Li, Xinghua Zhang, Yongkang Chen, Yibin Xie, Jiancheng Liu, Qiang Feng, Yi Wang, Wei Yuan, Jie Ma. G-CSF is a key modulator of MDSC and could be a potential therapeutic target in colitisassociated colorectal cancers[J]. Protein&Cell, 2016, 7(2): 130-140. doi: 10.1007/s13238-015-0237-2

G-CSF is a key modulator of MDSC and could be a potential therapeutic target in colitisassociated colorectal cancers

doi: 10.1007/s13238-015-0237-2
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This work was supported by the National Basic Research Program (973 Program) (No. 2014CB542103), Beijing Natural Science Foundation of China (Grant no.7144237), The Beijing Training Project for The Leading Talents (Z131107000513001), Beijing Nova Program (Z131107000413066) and the National Natural Science Foundation of China (Grant No. 81541154).

  • Received Date: 2015-09-29
  • Rev Recd Date: 2015-11-30
  • Granulocyte colony-stimulating factor (G-CSF) is an essential regulator of neutrophil trafficking and is highly expressed in multiple tumors. Myeloid derived suppressor cells (MDSCs) promote neoplastic progression through multiple mechanisms by immune suppression. Despite the findings of G-CSF function in colon cancer progression, the precise mechanism of G-CSF on MDSCs regulation and its blockade effects on tumor growth remains a worthy area of investigation. In this study we observed an overexpression of G-CSF in a mouse colitis-associated cancer (CAC) model, which was consistent with the accumulation of MDSCs in mouse colon tissues. Further in vitro studies demonstrated that G-CSF could promote MDSCs survival and activation through signal transducer and activator of transcription 3 (STAT3) signaling pathway. Moreover, compared with isotype control, anti-G-CSF mAb treatment demonstrated reduced MDSC accumulation, which led to a marked decrease in neoplasm size and number in mice. Our results indicated that G-CSF is a critical regulating molecule in the migration, proliferation and function maintenance of MDSCs, which could be a potential therapeutic target for colitis-associated cancer.
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