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. 2013 Aug 19;32(50):5614–5624. doi: 10.1038/onc.2013.322

Figure 2.

Figure 2

Loss of C/EBPβ is linked to the induction of EMT in response to TGF-β1. (a, c) Representative brightfield and immunofluorescence images showing induction of morphological characteristics of EMT and loss of nuclear staining of C/EBPβ in NMuMG cells (a) but not in EpH4 cells (c) after TGF-β1 treatment (10 ng/ml, 48 h). Scale bars, 50 μm. (b, d) Results from immunoblotting analysis showing changes in the expression of established EMT markers, and decreased expression of all three isoforms of C/EBPβ (LAP1, LAP2 and LIP) in NMuMG cells (b) but not in EpH4 cells (d) after TGF-β1 treatment (10 ng/ml, 48 h). (e) Immunoblotting analysis of the effect of TGF-β1 treatment (10 ng/ml, 1 h) on phosphorylation of Smad3 (p-Smad3) in NMuMG and EpH4 cells. (f) Immunoblotting analysis of the effect of siRNA-mediated knockdown of Smad3 (100 nM, 72 h) on the repression of C/EBPβ during TGF-β1-induced EMT (5 ng/ml, 24 h) in NMuMG cells. Calnexin was used as a loading control for all immunoblotting experiments.