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. 2016 Jan 31;2016:3543678. doi: 10.1155/2016/3543678

Figure 1.

Figure 1

The epithelial/mesenchymal status of MCs is due to the balance of signals delivered by multiple receptors. Stimuli promoting EMT are delivered by TGF-β in cooperation with inflammatory cytokines and other mediators such as IL-1β, IL-6, TLR ligands, AGEs, and angiotensin. Smad2/3 pathway plays a main role in combination with ERK1/2 and NF-κB pathway and all converge on the expression of Snail, the master gene of EMT. Integrin activation promotes the induction of conformational changes and the invasivity of MCs. On the other hand, signals delivered by BMP7 and HGF favor the epithelial phenotype through the activation of Smad1/5/8 and the inhibition of the Smad2/3 signaling. Also, signals delivered by cell-to-cell confluency (E-cadherin omotypic junctions) may lead to predominance of p38 MAPK over ERK1/2 and to the inhibition of NF-κB activity. Caveolin-1 organizes signaling platforms favoring the stability of membrane receptors and inhibiting the Ras/MEK/ERK1/2 pathway.