Regulation of the glucose metabolic enzymes by oxidative stress response factor Nrf2

Abstract

Nrf2 is a key factor in defense against oxidative stress, which is degraded through binding to Keap1. In cancer cells, aberrant Nrf2 activation through Keap1 mutation and the pentose phosphate pathway (PPP) as a source of nucleic acids promote proliferation, and glycolytic intermediates are required for PPP. In this study, we investigated the regulation of Glut1, and enzymes of glycolysis, TCA cycle and PPP by treatment of tBHQ (Keap1 inhibitor), Nrf2 knockdown or overexpression. As a result, we found that Glut1, PGD, TKT and G6PD levels are dependent on the Nrf2 expression level.