Genomics of signalling crosstalk of estrogen receptor alpha in breast cancer cells

ABSTRACT: The estrogen receptor a (ERa) is a ligand-regulated transcription factor. However, a wide variety of other extracellular signals can activate ERa in the absence of estrogen. The impact of these alternate modes of activation on gene expression profiles has not been characterized. We show that estrogen, growth factors and cAMP elicit surprisingly distinct ERa-dependent transcriptional responses in human MCF7 breast cancer cells. In response to growth factors and cAMP, ERa primarily activates and represses genes, respectively. The combined treatments with the antiestrogen tamoxifen and cAMP or growth factors regulate yet other sets of genes. In many cases, tamoxifen is perverted to an agonist, potentially mimicking what is happening in certain tamoxifen-resistant breast tumors and emphasizing

ORGANISM(S): Homo sapiens

SUBMITTER: Peter Dudek 

PROVIDER: E-GEOD-10466 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress