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Figure 7 | Breast Cancer Research

Figure 7

From: Reversal by RARα agonist Am580 of c-Myc-induced imbalance in RARα/RARγ expression during MMTV-Myc tumorigenesis

Figure 7

Analysis of tumors from Am580-treated and untreated control mice. A) Immunoblotting analyses for E-cadherin, retinoic acid receptor (RAR)α, RARγ, phosphorylated Erk (activation) and p27 levels of 4-[(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)carboxamido]benzoic acid (Am580)-responsive (Am580 R) and -nonresponsive (Am580 NR) tumors (three representatives from each group of five tumors shown). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as a loading control. B) Immunohistochemical analyses of RARα-responsive genes Cyp26A, E-cadherin and p27 (brown staining) in sections from (Am580 R, Am580 NR and Myc-Ctrl tumors; scale bar = 200 μm. C) Immunohistochemical analysis for CRBP1 expression in tumor sections indicates that tumors from Am580 R mice expressed CRBP1, whereas only stromal cells in tumor sections from the Am580 NR and Myc-Ctrl mice expressed CRBP1 (black arrows). Am580 R tumor sections had small nodules of CRBP1-negative cells (white arrows); bar = 400 μm. D) H & E staining of a Myc-Ctrl tumor section reveals an invasive carcinoma with very few necrotic areas, whereas a section from an Am580 NR tumor displays an increase in frequency of necrosis (white arrows; bar = 200 μm) and that from an Am580 R tumor displays larger and more necrotic areas (white arrows; bar = 400 μm). Sections shown are representative of five replicates. Immunohistochemical analysis was done on sections from eight tumors per experimental group.

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