Abstract
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.
Highlights
Estrogen receptor-α (ERα) is a key regulator of proliferation, growth, differentiation, development and maintenance of a wide range of tissues including the mammary glands
We have previously shown that in estrogen-responsive MCF-7 breast cancer cells, glycogen synthase kinase-3β (GSK-3β), a serine kinase involved in the regulation of a multitude of cellular functions, interacts with and stabilizes ERα in the cytoplasm of cells in the absence of E2 [8,9]
We first investigated whether E2 treatment has an impact on intracellular β-catenin localization and whether there is a physical interaction of β-catenin and ERα in breast cancer cells
Summary
Estrogen receptor-α (ERα) is a key regulator of proliferation, growth, differentiation, development and maintenance of a wide range of tissues including the mammary glands. It has been implicated in various pathological processes including breast cancer. We have previously shown that in estrogen-responsive MCF-7 breast cancer cells, glycogen synthase kinase-3β (GSK-3β), a serine kinase involved in the regulation of a multitude of cellular functions, interacts with and stabilizes ERα in the cytoplasm of cells in the absence of E2 [8,9]. We were interested to investigate the potential physical and functional interaction between β-catenin and ERα in breast cancer cells
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