P53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production.

ABSTRACT:

Background

The p53 tumor suppressor protein is a transcription factor that initiates transcriptional programs aimed at inhibiting carcinogenesis. p53 represses metabolic pathways that support tumor development (such as glycolysis and the pentose phosphate pathway (PPP)) and enhances metabolic pathways that are considered counter-tumorigenic such as fatty acid oxidation.

Findings

In an attempt to comprehensively define metabolic pathways regulated by p53, we performed two consecutive high-throughput analyses in human liver-derived cells with varying p53 statuses. A gene expression microarray screen followed by constraint-based modeling (CBM) predicting metabolic changes imposed by the transcriptomic changes suggested a role for p53 in enhancing gluconeogenesis (de novo synthe

SUBMITTER: Goldstein I 

PROVIDER: S-EPMC4178212 | biostudies-literature | 2013 Feb

REPOSITORIES: biostudies-literature