ABOUT THE COVER
These are overlaid confocal microscopy images of E-cadherin, Actin and DAPI staining in fibronectin-depleted MCF-10A-Ca1h (Ca1h) breast cancer cells. In the article, beginning on page 1579, Shinde and colleagues demonstrate that wild type Ca1h cells are not metastatic, express high amounts of intracellular fibronectin, and display a very mesenchymal phenotype. In contrast, when fibronectin is depleted from the Ca1h cells they undergo a mesenchymal-epithelial transition (as shown) characterized by a return of junctional E-cadherin expression and an enhanced ability to form pulmonary tumors following tail vein injection. As opposed to the tumor promoting role of fibronectin in the extracellular matrix, this study suggests that when epithelial-derived carcinoma cells undergo epithelial-mesenchymal transition, constitutive expression of fibronectin stabilizes their mesenchymal phenotype and inhibits the cell autonomous ability of those cells to complete the final steps of the metastatic process.