Abstract
Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to ‘heal’ damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.
Highlights
Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases
From all the work carried out in the context of organ fibrosis and cancer we can conclude that the pathways and players identified that lead to pathological EMTs are basically the same
Both in cancer and fibrosis TGF-b1, TNF-a and hypoxia cooperate in the triggering of EMT, converging in the induction of Snail activity through different mechanisms among which the activation of NF-kB seems to play a central role
Summary
Inflammation and cancer The link between cancer and inflammation has been recognized for decades, as strong associations have been established between chronic inflammatory conditions and tumourigenesis (Cordon-Cardo & Prives, 1999). Among the transcription factors involved in the induction of EMT, Snail factors have been associated with renal fibrosis and significantly, TGF-b1 is the most potent inducer of Snail transcription (Fig 3) The expression of these genes increases in the obstructed kidney after UUO (Sato et al, 2003; Tan et al, 2006; Yoshino et al, 2007) and Snail activation is sufficient to induce EMT and all the hallmarks of kidney fibrosis in adult mice (Boutet et al, 2006). Data from many laboratories indicate that Snail factors are crucial mediators of TGF-b1-induced EMT
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