Matrix metalloproteases and epithelial-to-mesenchymal transition : Implications for carcinoma metastasis

The epithelial to mesenchymal transition (EMT) is characterized by the loss of epithelial characteristics and the gain of mesenchymal attributes in epithelial cells. It has been associated with physiological and pathological processes requiring epithelial cell migration and invasion. Initially, EMT was observed in embryological and adult development with many well characterized examples including the conversions of epiblast to primary mesenchyme (gastrulation), somite to sderotome, somite to dermis, myotome to migratory myoblast, dorsal neural tube to neural crest, placodal ectoderm to cranial ganglion precursor, intermediate mesoderm to nephric mesenchyme, lateral mesoderm to connective/muscular tissue, endocardium to cardiac cushion mesenchyme and trophectoderm invasion.[1],[2] In addition, evidence is mounting to support an important role of EMT pathways in the progression of carcinoma to metastasis providing epithelial tumour cells with the ability to migrate, invade the surrounding stroma and disseminate in secondary organs.[3]–[5