Additional file 1: of Foxf2 plays a dual role during transforming growth factor beta-induced epithelial to mesenchymal transition by promoting apoptosis yet enabling cell junction dissolution and migration

Figure S1. Foxf2 expression is upregulated during EMT via the canonical Smad pathway. The increased expression of Foxf2 during an EMT was assessed in normal murine mammary gland epithelial cells (NMuMG) and in murine and human breast cancer cells. Figure S2. Foxf2 is required for TGFβ-induced disruption of adherens junctions. RNAi-mediated ablation prevents an EMT as visualized by immunofluorescence staining for epithelial and mesenchymal markers. Figure S3. Foxf2 regulates the expression of Zeb1, Zeb2, Id2, and members of the miR-200 family as determined by quantitative RT-PCR of their expression during an EMT in the absence of presence of Foxf2. Figure S4. Foxf2 regulates Noxa expression and thus affects cell proliferation and apoptosis. Foxf2 regulated the expression of Noxa, and siRNA-mediated depletion of Noxa prevented an increase in cell death induced by the loss of Foxf2 expression as assessed by quantitative RT-PCR. Figure S5. EGF ligand-mediated EGF receptor signaling overcomes Foxf2-controlled cell survival. Foxf represses the expression of EGF receptor ligands as assessed by quantitative RT-PCR. Supplementary material and methods. Detailed information is given on the antibodies and reagents, on biochemical and cell biological methods, and on RNA sequencing and bioinformatics analysis used in the study. Table S1. Excel file summarizing the differential expression analysis (siFoxf2 to siCtrl after 4 days TGFβ treatment or siCtrl with vs without TGFβ for 4 days) of all transcripts detected with RNA-sequencing. Table S2. Excel file showing the list of genes belonging to the different gene signatures (modules) and the strength of their modular membership (kME values). (ZIP 14675 kb)