Additional file 5: Figure S2. of Expression profiling of in vivo ductal carcinoma in situ progression models identified B cell lymphoma-9 as a molecular driver of breast cancer invasion

BCL9 showed increased nuclear expression, while BCL9L expression remained cytoplasmic during ductal carcinoma in situ (DCIS) invasive transition. A Immunofluorescence staining of BCL9 (red; top panel), BCL9L (red; bottom panel), K5/K19 (green), and Hoechst (blue) in a primary sample that represents: adjacent normal glands (left), DCIS lesions (middle), and invasive ductal carcinoma (IDC) (right). BCL9 and BCL9L are conjugated to Alexa-Fluor 594 (red) and K5/K19 were conjugated to Alexa-Fluor 488 (green). Nuclei were counterstained with Hoechst. Scale bars 50 μm, × 40 objective was used. B, C RT-qPCR of BCL9 and BCL9L mRNA in epithelial cell adhesion molecule (EpCAM)-positive epithelial cells sorted from SUM225 (B) and DCIS.COM (C) mouse intraductal xenograft model (MIND) xenografts at 2, 6, and 10 weeks post-intraductal injection. The bar graphs represent fold change normalized to 2 weeks. Data are mean values ± standard error of the mean (n = 3, *p <0.05). D Representative western blot analysis of cell lysates from control and BCL9-KD-SUM225 and DCIS.COM blotted with anti-BCL9, and anti-BCL9L antibodies. β-actin was used as a loading control. The analysis showed no change in BCL9L protein levels in BCL9-KD cells compared to control cells. (PDF 5012 kb)