Journal
PROTEIN & CELL
Volume 7, Issue 2, Pages 130-140Publisher
SPRINGEROPEN
DOI: 10.1007/s13238-015-0237-2
Keywords
inflammation; cancer; granulocyte colony-stimulating factor; myeloid derived suppressor cells
Categories
Funding
- National Basic Research Program (973 Program) [2014CB542103]
- Beijing Natural Science Foundation of China [7144237]
- Beijing Training Project for The Leading Talents [Z131107000513001]
- Beijing Nova Program [Z131107000413066]
- National Natural Science Foundation of China [81541154]
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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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