Investigation of mechanisms for the regulation of CD8 T cell exhaustion by type 2 diabetic drug, metfromin

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K18452
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Tumor therapeutics
• Research Institution: Okayama University
• Principal Investigator: Eikawa Shingo 岡山大学, 医歯薬学総合研究科, 助教 (40635265)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: CD8 T細胞 / 代謝免疫 / メトホルミン / 好気的解糖 / グルコース / アミノ酸

Outline of Final Research Achievements

We previously argued that type 2 diabetic drug, metformin has an anti tumor effect mediated by the modulation of CD8 T cell function. In this study, we investigated further mechanisms of the effect on several mouse tumor implantation model. These results revealed the activation of AMPK in antigen-specific CD8 T cell by metformin is quite important for tumor regression. Metformin-induced AMPK activation led to enhance an aerobic glycolysis of CD8 T cell through cell membrane translocation of amino acid transpoter, LAT1. These data indicated CD8 T cell metabolism has an critical role for anti-tumor effect of metformin.

Free Research Field

がん免疫