Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Oct 5;10(10):371. doi: 10.3390/cancers10100371

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Model of the regulation of the ESR1 gene expression and DNA methylation by PR in hormone-free breast cancer cells. In hormone-free ER+/PR+ breast cancer cells, PR binds to the low-methylated gene promoter, as well as to an enhancer-like intronic sequence of ESR1. PR binding at the gene promoter is required for maintaining ESR1 transcription. In the absence of PR, DNA methylation (mC) increases at the ESR1 promoter, and ESR1 transcription is reduced. Re-expression of PR in PR-depleted cells leads to PR binding to the low-methylated enhancer-like intronic sequence, but the high level of DNA methylation (mC) at the ESR1 promoter impedes PR binding to this genomic region. Consequently, re-expression of PR in PR-depleted cells is insufficient to restore ESR1 expression.