A New Role for ERα: Silencing via DNA Methylation of Basal, Stem Cell, and EMT Genes.

ABSTRACT: Resistance to hormonal therapies is a major clinical problem in the treatment of estrogen receptor α-positive (ERα⁺) breast cancers. Epigenetic marks, namely DNA methylation of cytosine at specific CpG sites (5mCpG), are frequently associated with ERα⁺ status in human breast cancers. Therefore, ERα may regulate gene expression in part via DNA methylation. This hypothesis was evaluated using a panel of breast cancer cell line models of antiestrogen resistance. Microarray gene expression profiling was used to identify genes normally silenced in ERα⁺ cells but derepressed upon exposure to the demethylating agent decitabine, derepressed upon long-term loss of ERα expression, and resuppressed by gain of ERα activity/expression. ERα-dependent DNA methylation targ

SUBMITTER: Ariazi EA 

PROVIDER: S-EPMC5308451 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature