Fig. 2

Foxf2 regulates cell migration and the expression of E-cadherin transcriptional repressors. a Phase-contrast micrographs of NMuMG cells stably expressing a control shRNA (shCtrl) or a Foxf2-specific shRNA (shFoxf2 703, 704) treated with transforming growth factor (TGF)β for 20 days. Scale bar = 100μm. b shRNA-mediated ablation of Foxf2 leads to sustained E-cadherin expression after 19 days of TGFβ treatment shown by immunoblotting analysis in shFoxf2 and shCtrl NMuMG cells. Tubulin was used as a loading control. c Foxf2 and d E-cadherin mRNA levels were determined by quantitative RT-PCR in shFoxf2 and shCtrl NMuMG cells treated with TGFβ for 19 days. Values were normalized to RPL19 and reported as fold changes compared with untreated shCtrl NMuMG cells. e Depletion of Foxf2 leads to reduced cell migration of NMuMG cells treated for 19 days with TGFβ through transwell filters compared with control cells (shCtrl). mRNA levels of f Zeb1, g Zeb2, and h Id2 were determined by quantitative RT-PCR in shFoxf2- and shCtrl-transfected NMuMG cells. Values were normalized to RPL19 and reported as fold changes compared with untreated shCtrl NMuMG cells. Data are shown as mean ± SEM of three independent experiments. Statistical values were calculated using a paired two-tailed t test between shCtrl and shFoxf2 cells. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001