Genomics of signaling crosstalk of estrogen receptor alpha in breast cancer cells.

ABSTRACT:

Background

The estrogen receptor alpha (ERalpha) is a ligand-regulated transcription factor. However, a wide variety of other extracellular signals can activate ERalpha in the absence of estrogen. The impact of these alternate modes of activation on gene expression profiles has not been characterized.

Methodology/principal findings

We show that estrogen, growth factors and cAMP elicit surprisingly distinct ERalpha-dependent transcriptional responses in human MCF7 breast cancer cells. In response to growth factors and cAMP, ERalpha primarily activates and represses genes, respectively. The combined treatments with the anti-estrogen tamoxifen and cAMP or growth factors regulate yet other sets of genes. In many cases, tamoxifen is perverted to an agonist, potentially mimicking

SUBMITTER: Dudek P 

PROVIDER: S-EPMC2268000 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature