Glucose Starvation-Induced Rapid Death of Nrf1α-Deficient, but Not Nrf2-Deficient, Hepatoma Cells Results from Its Fatal Defects in the Redox Metabolism Reprogramming.

ABSTRACT: Metabolic reprogramming exists in a variety of cancer cells, with the most relevance to glucose as a source of energy and carbon for survival and proliferation. Of note, Nrf1 was shown to be essential for regulating glycolysis pathway, but it is unknown whether it plays a role in cancer metabolic reprogramming, particularly in response to glucose starvation. Herein, we discover that Nrf1α^-/- hepatoma cells are sensitive to rapid death induced by glucose deprivation, such cell death appears to be rescued by Nrf2 interference, but HepG2 (wild-type, WT) or Nrf2^-/- cells are roughly unaffected by glucose starvation. Further evidence revealed that Nrf1α^-/- cell death is resulted from severe oxidative stress arising from aberran

SUBMITTER: Zhu YP 

PROVIDER: S-EPMC7407023 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature