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• W2034199555 abstract "Background: We have previously shown that overexpression of metastasis associated protein 2 (MTA2) can render estrogen receptor (ER)-positive breast cancer cells hormone-independent through postranscriptional effects on ER acetylation and phosphorylation. Recently we discovered that MTA2 overexpression in ER-negative MDA-MB-231 breast cancer cells enhances invasion and metastasis in athymic nude mice which involves activation of the Rho pathway. It is also known that the androgen receptor (AR) is frequently expressed in breast tumors; however its role in proliferation, invasion, or breast cancer metastasis is poorly understood. Materials and Methods: MTA2 was stably overexpressed in MDA-MB-231 and its levels validated using Western blot analysis. To identify downstream effects due to MTA2 overexpression, we employed reverse phase protein arrays, and Affymetrix expression arrays. Significant changes in gene expression were identified using dCHIP software, and student t tests. Invasion was examined using modified Boyden chamber growth assays, proliferation was assayed using soft agar growth and MTT assays, and metastasis was measured as tumor growth in athymic nude mice. Results: MTA2 overexpression in ER-negative cells enhanced distant and skin metastases in athymic nude mice. In an attempt to identify effectors of MTA2-mediated metastasis, we used RNA microarray and protein array screens, and found that AR was significantly increased. As a control, we employed a rescue of the highly metastatic MTA2-MDA-MB-231 cell phenotype via stable transfection and add-back of Rho GDIa, a gene that was concomitantly down-regulated with MTA2 overexpression. AR levels were significantly reduced with Rho GDIa add-back. To determine if AR was functional in these cells, we used ARE-luciferase reporter assays and discovered that both basal, and agonist (R1881)-induced transcriptional activity were significantly enhanced. The AR antagonist, bicalutamide, was effective at significantly decreasing the invasive potential of MTA2- overexpressing MDA-MB-231 cells In vivo experiments in nude mice with bicalutamide treatment are underway. Discussion: AR was significantly overexpressed with the aggressive phenotype conferred via MTA2 overexpression. This suggests that blockade of AR action might provide a new therapeutic target to inhibit metastasis of breast cancer cells. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P5-06-01." @default.
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• W2034199555 date "2010-12-15" @default.
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• W2034199555 title "Abstract P5-06-01: MTA2 and AR Overexpression in ER-Negative Breast Cancer Cells: Roles in Invasion and Metastasis" @default.
• W2034199555 doi "https://doi.org/10.1158/0008-5472.sabcs10-p5-06-01" @default.
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