Fig. 3
From: Somatic loss of estrogen receptor beta and p53 synergize to induce breast tumorigenesis
Expression of ERβ in normal mammary gland and p53-deficient mammary tumors. a RT-PCR analysis of total RNA from mammary glands of 8-week-old K14CreERβ F/F and ERβ F/F (control) female mice as well as mammary tumors from K14Crep53 F/F and K14CreERβ F/F p53 F/F female mice with primers that amplify the exon 3 of ERβ cDNA. Of note, a decline of ERβ expression during tumor development is demonstrated by the decreased levels of the ERβ transcript in p53-deficient mammary tumors of K14Crep53 F/F mice compared with the normal mammary glands of the control mice (lane 7 vs lanes 1 and 2). Graph represents quantification of the band intensities of ERβ exon 3 cDNA in RT-PCR analysis (normalized to that of the normal mammary gland in lane 7). b Sections containing normal mammary gland of 8-week-old ERβ F/F female mouse (a) and mammary tumors from K14Crep53 F/F (b, c) and K14CreERβ F/F p53 F/F (d) female mice were stained for ERβ. Nuclei of the epithelial cells of the normal duct present strong staining (a). Inset image displays enlargement of the denoted duct. Scale bars, 100 μm (inset 50 μm). Microphotographs of tumor sections b and c are from the same ERβ-positive tumor from K14Crep53 F/F mice (developed in the absence of p53). Compared with the mammary gland (a), there is weaker staining in the nuclei of the tumor epithelial cells (b) consistent with the difference in ERβ mRNA levels in a. In addition, within the same tumor, there is reduced expression of ERβ in poorly differentiated epithelial cells (c) compared with the tumor component with more intact cell polarity (b). Lack of ERβ expression is observed in mammary tumors from K14CreERβ F/F p53 F/F mice (d). c Breast tumor cells with ERα-positive nuclei in K14Crep53 F/F (left) and K14CreERβ F/F p53 F/F (right) mice. Inset image shows enlargement of the denoted tumor area. Scale bars, 100 μm. ER estrogen receptor