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. Author manuscript; available in PMC: 2013 Sep 11.
Published in final edited form as: Nat Cell Biol. 2009 Jul 13;11(8):943–950. doi: 10.1038/ncb1905

Figure 4. SNAIL1 and SMAD3/4 play essential and cooperative roles as transcriptional repressors of junction components during EMT.

Figure 4

(a, b) RNA analysis of the effect of siRNA mediated silencing of SNAIL1 and SMAD4 in NMuMG cells in untreated and TGF-β treated NMuMG cells (24 h). (c-e) Effect of SNAIL1 and SMAD4 siRNAs on CAR, occludin and E-cadherin mRNA levels during TGF-β induced EMT. Data indicate mean ± SEM and are representative of three independent experiments. *, P < 0.05, different from untreated cells. §, P < 0.05, different from TGF-β + control siRNA. †, P < 0.05, different from TGF-β + SNAIL1 siRNA. (f) Effect of SMAD3 inhibition on CAR and E-cadherin mRNA levels during TGF-β induced EMT. *, P < 0.05, different from untreated cells. §, P < 0.05, different from TGF-β treatment. Data represent mean ± SEM of three independent experiments. (g) Cooperation of SNAIL1 and SMAD3/4 transcription factors during TGF-β-induced EMT. SNAIL1 and SMAD3/4 interact and form a transcriptional repressor complex, which is targeted to adjacent Eboxes (E) and SBE sites in genes encoding junction proteins like CAR, occludin and E-cadherin. As a result, these genes are repressed.