Estradiol-17β Upregulates Pyruvate Kinase M2 Expression to Coactivate Estrogen Receptor-α and to Integrate Metabolic Reprogramming With the Mitogenic Response in Endometrial Cells

Abstract

We show for the first time that E2-induced hESC proliferation is associated with a shift in glucose metabolism toward aerobic glycolysis, and the molecular basis for this metabolic shift is linked to the effects of E2 on PKM2. In addition, PKM2 acts as a transcriptional coactivator for ERα and small-molecule PKM2 activators inhibit ERα transcriptional activity and reduce E2-induced cell proliferation.