Abstract
Cancer cells are well known for their high glycolysis, which produces NADH in the cells. Otto Warburg postulated that this change in metabolism is the fundamental cause of cancer. Many substances have been developed to inhibit glycolysis, and such glycolytic inhibitors are currently the subject of intense research as anticancer agents. Carboxyl‐terminal binding protein (CtBP) was initially identified by virtue of its ability to interact with E1A, the major transforming protein of adenovirus. Our work has uncovered CtBP being the first NADH‐sensing transcriptional regulator in mammals. We found that NADH binding to CtBP stimulates the CtBP interaction with transcription repressors and cellular perturbations that affect the ratio of free NAD+/NADH regulate the ability of CtBP to interact with its binding partners. As a foe of multiple tumor suppressors, CtBP promotes EMT and functions as apoptosis antagonist. The unique function of this protein as a redox‐sensor in transcription control allows cells to couple the metabolic status with gene expression, contributing to tumor progression. This work was supported by NIH grant R01CA115468.
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