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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: COUP-TFII inhibits NFkappaB activation in endocrine-resistant breast cancer cells.

Authors: Litchfield, Lacey M; Appana, Savitri N; Datta, Susmita; Klinge, Carolyn M

Published In Mol Cell Endocrinol, (2014 Jan 25)

Abstract: Reduced COUP-TFII expression contributes to endocrine resistance in breast cancer cells. Endocrine-resistant breast cancer cells have higher NFkappa B (NFκB) activity and target gene expression. The goal of this study was to determine if COUP-TFII modulates NFκB activity. Endocrine-resistant LCC9 cells with low endogenous COUP-TFII displayed ∼5-fold higher basal NFκB activity than parental endocrine-sensitive MCF-7 breast cancer cells. Transient transfection of LCC9 cells with COUP-TFII inhibited NFκB activation and reduced NFκB target gene expression. COUP-TFII and NFκB were inversely correlated in breast cancer patient samples. Endogenous COUP-TFII coimmunoprecipitated with NFκB subunits RelB and NFκB1 in MCF-7 cells. COUP-TFII inhibited NFκB-DNA binding in vitro and impaired coactivator induced NFκB transactivation. LCC9 cells were growth-inhibited by an NFκB inhibitor and 4-hydroxytamoxifen compared to MCF-7 cells. Together these data indicate a novel role for COUP-TFII in suppression of NFκB activity and explain, in part, why decreased COUP-TFII expression results in an endocrine-resistant phenotype.

PubMed ID: 24141032 Exiting the NIEHS site

MeSH Terms: Breast Neoplasms/genetics; Breast Neoplasms/metabolism*; COUP Transcription Factor II/metabolism*; DNA, Neoplasm/metabolism; Drug Resistance, Neoplasm/drug effects*; Drug Resistance, Neoplasm/genetics; Female; Gene Expression Regulation, Neoplastic/drug effects; Hormones/pharmacology*; Humans; Imidazoles/pharmacology; MCF-7 Cells; NF-kappa B/metabolism*; Phosphorylation/drug effects; Protein Binding/drug effects; Protein Binding/genetics; Protein Subunits/genetics; Protein Subunits/metabolism; Quinoxalines/pharmacology; RNA, Messenger/genetics; RNA, Messenger/metabolism; Signal Transduction/drug effects; Signal Transduction/genetics; Transcription Factor RelA/metabolism

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