KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression.

ABSTRACT:

Background

Histone deacetylases (HDACs) engage in the regulation of various cellular processes by controlling global gene expression. The dysregulation of HDACs leads to carcinogenesis, making HDACs ideal targets for cancer therapy. However, the use of HDAC inhibitors (HDACi) as single agents has been shown to have limited success in treating solid tumors in clinical studies. This study aimed to identify a novel downstream effector of HDACs to provide a potential target for combination therapy.

Methods

Transcriptome sequencing and bioinformatics analysis were performed to screen for genes responsive to HDACi in breast cancer cells. The effects of HDACi on cell viability were detected using the MTT assay. The mRNA and protein levels of genes were determined by quantitative re

SUBMITTER: Wei H 

PROVIDER: S-EPMC8441056 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature