[beta]-Catenin Is a Positive Regulator of Estrogen Receptor-[alpha] Function in Breast Cancer Cells

• Published in: Cancers Vol. 3; no. 3; p. 2990
• Main Authors: Gupta, Nibedita, Schmitt, Fee, Grebhardt, Sina, Mayer, Doris
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01-09-2011
• Subjects: Breast cancer; Cytoplasm; Estrogens; Kinases; Phosphorylation; Proteins; Signal transduction
• DOI: 10.3390/cancers3032990
• EISSN: 2072-6694

Estrogen receptor-alpha (ERα) is a key factor in the development of breast cancer in humans. The expression and activity of ERα is regulated by a multitude of intracellular and extracellular signals. Here we show a cross-talk between β-catenin and ERα in human breast cancer cells. Knockdown of β-catenin by RNAi resulted in significant reduction of ERα mRNA and/or protein levels in MCF-7, T-47D, and BT-474 breast cancer cells and in significant reduction of estradiol-induced expression of the ERα target genes pS2 and GREB1. In addition β-catenin silencing resulted in significant decrease of growth of MCF-7 cells both in the absence and presence of estradiol. β-catenin and ERα could not be co-immunoprecipitated by ERα antibodies from lysates of E2-treated or untreated cells suggesting lack of direct physical interaction. It is concluded that β-catenin is a positive regulator of ERα mRNA and protein expression.