EMSY enhances glycolysis in ovarian cancer cells

Abstract

EMSY is critical in the progression of ovarian cancer; nevertheless, its impact on tumor metabolism is not widely known. This study showed ovarian cancer cells overexpressing EMSY produce more lactate and have upregulated LDHA expression; the promoting effect of EMSY on the malignant phenotype of these cells is eliminated when LDHA expression is knocked down or glycolysis is inhibited in ovarian cancer cells. Mechanistic studies revealed that EMSY interacts with β-catenin, and the knockdown of EMSY inhibits the transcriptional activation of LDHA by β-catenin. In summary, this study identifies EMSY’s metabolic regulatory role in ovarian cancer cells and offers treatment of ovarian cancer with a new therapeutic target.