Reversal of obesity-driven aggressiveness of endometrial cancer by metformin.

Abstract

The obese state promoted tumor aggressiveness in the LKB1^fl/fl p53^fl/fl mouse model, accompanied by increases in energy metabolism, lipid biosynthesis, and markers of lipid peroxidation. Metformin had increased efficacy against endometrial cancer in obese <i>versus</i> lean mice and reversed the detrimental metabolic effects of obesity in the endometrial tumors. Taken together, it is likely that the unique metabolic milieu underlies metformin's improved efficacy in treating endometrial cancer which develop in an obese host environment.