Epithelial outgrowth from cells treated with HGF or KGF showed similar expression patterns for Krt3 and Krt14. However, p63 was highly expressed by KGF-treated limbal epithelial sheets but not by those treated with HGF. Kinase inhibitor studies showed that induction of DNp63aexpression by KGF is mediated via the p38 pathway. Their results and ours indicate that phosphorylation and activation of the Ras/Raf/mitogen-activated protein kinase pathway leads to phosphorylation of regulatory proteins and transcription factors, culminating in cell migration, proliferation, and/or differentiation both in basal epithelial cells of the RK wound and cells grown from limbal explant culture. In conclusion, we propose that the phenotypic changes in basal corneal epithelial cells in the CUCC, which expresses the limbal SC markers on disrupted BM and Bowman��s membrane, might be due to an alteration of their niche, including the extracellular matrix and the BM. Fibroblasts are the most abundant cell type found in the stroma Diperodon surrounding glandular epithelial tissues. Ample evidence indicates that fibroblasts can promote epithelial tumor progression via paracrine signaling, but direct contact with invading tumor cells may affect tumorigenesis and metastasis as well. Recent evidence has shown that fibroblasts and epithelial cells can form heterotypic cell-cell adhesions in vitro, and that cadherin adhesion molecules are recruited to these heterotypic adhesions. Metastatic tumor cells often show changes in cadherin expression.To determine if cadherin-23 plays a role in adhesion, we performed adhesion assays after disruption of cadherin-23 with inhibitory antibodies or after knockdown of the protein by RNAi. Many tumor cells undergo a ����cadherin switch���� in which E-cadherin expression decreases and N-cadherin expression increases, although changes in other cadherins may also be observed. These changes in cadherin expression are associated with the Kaempferide decreased adhesion and increased motility characteristic of metastatic disease. Cadherin-23 is an atypical cadherin implicated in several deafness syndromes due to its role as a component of the tip link complex between stereocilia in cochlear hair cells.