Translational offsetting as a mode of estrogen receptor ?-dependent regulation of gene expression

ABSTRACT: Estrogen receptor alpha (ER?) activity is associated with increased cancer cell proliferation. Studies aiming to understand the impact of ER? on cancer-associated phenotypes have largely been limited to its transcriptional activity. Herein, we demonstrate that ER? coordinates its transcriptional output with selective modulation of mRNA translation. Importantly, translational perturbations caused by depletion of ER? largely manifest as "translational offsetting" of the transcriptome, whereby amounts of translated mRNAs and corresponding protein levels are maintained constant despite changes in mRNA abundance. Transcripts whose levels, but not polysome-association, are reduced following ER? depletion lack features which limit translation efficiency including structured 5'UTRs and miRNA targe

SUBMITTER: Julie Lorent 

PROVIDER: S-SCDT-EMBOJ-2018-101323 | biostudies-other |

REPOSITORIES: biostudies-other