TIGAR induces p53-mediated cell-cycle arrest by regulation of RB-E2F1 complex.

ABSTRACT:

Background

p53 induces cell-cycle arrest and apoptosis in cancer cells and negatively regulates glycolysis via TIGAR. Glycolysis is crucial for cancer progression although TIGAR provides protection from reactive oxygen species and apoptosis. The relation between TIGAR-mediated inhibition of glycolysis and p53 tumour-suppressor activity is unknown.

Methods

RT-PCR, western blot, luciferase and chromatin immunoprecipitation assays were used to study TIGAR gene regulation. Co-IPP was used to determine the role of TIGAR protein in regulating the protein-protein interaction between retinoblastoma (RB) and E2F1. MCF-7 tumour xenografts were utilised to study the role of TIGAR in tumour regression.

Results

Our study shows that TIGAR promotes p21-independent, p53-mediated G1-p

SUBMITTER: Madan E 

PROVIDER: S-EPMC3405207 | biostudies-literature | 2012 Jul

REPOSITORIES: biostudies-literature