Vergara D.,Laboratoire Of Neuroimmunologie Des Annelides |
Merlot B.,Laboratoire Of Neuroimmunologie Des Annelides |
Lucot J.-P.,Laboratoire Of Neuroimmunologie Des Annelides |
Collinet P.,Laboratoire Of Neuroimmunologie Des Annelides |
And 3 more authors.
Cancer Letters | Year: 2010
Ovarian cancer is a highly metastatic disease and the leading cause of death from gynecologic malignancy. Hence, and understanding of the molecular changes associated with ovarian cancer metastasis could lead to the identification of targets for novel therapeutic interventions. The conversion of an epithelial cell to a mesenchymal cell plays a key role both in the embryonic development and cancer invasion and metastasis. Cells undergoing epithelial-mesenchymal transition (EMT) lose their epithelial morphology, reorganize their cytoskeleton and acquire a motile phenotype through the up- and down-regulation of several molecules including tight and adherent junctions proteins and mesenchymal markers. EMT is believed to be governed by signals from the neoplastic microenvironment including a variety of cytokines and growth factors. In ovarian cancer EMT is induced by transforming growth factor-β (TGF-β), epidermal growth factor (EGF), hepatocyte growth factor (HGF) and endothelin-1 (ET-1). Alterations in these cellular pathways candidate them as useful target for ovarian cancer treatment. © 2009 Elsevier Ireland Ltd. Source