WRN modulates translation by influencing nuclear mRNA export in HeLa cancer cells.

ABSTRACT:

Background

The Werner syndrome protein (WRN) belongs to the RecQ family of helicases and its loss of function results in the premature aging disease Werner syndrome (WS). We previously demonstrated that an early cellular change induced by WRN depletion is a posttranscriptional decrease in the levels of enzymes involved in metabolic pathways that control macromolecular synthesis and protect from oxidative stress. This metabolic shift is tolerated by normal cells but causes mitochondria dysfunction and acute oxidative stress in rapidly growing cancer cells, thereby suppressing their proliferation.

Results

To identify the mechanism underlying this metabolic shift, we examined global protein synthesis and mRNA nucleocytoplasmic distribution after WRN knockdown. We determined tha

SUBMITTER: Iglesias-Pedraz JM 

PROVIDER: S-EPMC7557079 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature