Interplay between AP-1 and ERalpha in regulating gene expression and proliferation networks in breast cancer cells

ABSTRACT: Estrogen receptor alpha (ERalpha) is a ligand-dependent transcription factor that plays an important role in breast cancer. Estrogen-dependent gene regulation by ERalpha can be mediated by interaction with other DNA-binding proteins, such as activator protein-1 (AP-1). The nature of such interactions in mediating the estrogen response in breast cancer cells remains unclear. Here we show that knockdown of c-Fos, a component of the transcription factor AP-1, attenuates the expression of 37% of all estrogen-regulated genes, suggesting that AP-1 is a fundamental factor for ERalpha-mediated transcription. Additionally, knockdown of c-Fos affected the expression of a number of genes that were not regulated by estrogen. Pathway analysis reveals that silencing of c-Fos downregulates an E2F1-depend

ORGANISM(S): Homo sapiens

SUBMITTER: Chunyan Zhao 

PROVIDER: E-GEOD-36586 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress