Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 120, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2019.109458
Keywords
Metformin; Granulocytic myeloid-derived suppressor cell; Colon cancer cell; Tumor-Bearing mice
Funding
- Jiangsu Province's Key Medical Talents Program [ZDRCB2016018]
- Summit of the Six Top Talents Program of Jiangsu Province [2015-WSN-116]
- Specialized Project for Clinical Medicine of Jiangsu Province [BL2014065]
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Metformin, an oral medicine broadly used for the treatment of type 2 diabetes, has been found to significantly improve tumor incidence and survival in large-scale clinical analysis. In recent years, the antitumor effect and mechanism of metformin have received much attention. Myeloid-derived suppressor cells (MDSCs), a major immunosuppressive cell type that accumulates in tumor-bearing hosts, can inhibit T cells and promote tumor immune escape. The mechanism by which metformin exerts its anti-tumor effect by regulating MDSCs remains unclear. Here, we found that metformin could inhibit the accumulation and suppressive capacity of G-MDSCs, delay tumor progression and elicit Th1 and CTL responses in murine colon cancer CT-26 cell-transplanted mice. In additionally, metformin could enhance the phosphorylation of AMPK, reduce STAT3 phosphorylation levels, and down-regulate the inhibitory function of G-MDSCs in vitro. These results suggest that metformin may be a potential clinical benefit for antitumor immunotherapy in tumor-bearing mice.
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