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promoter activity exclusively in oral keratinocytes but not in OSCC cells. The effect of EGF on TGFβ1-mediated Smad-driven promoter activity and N-cadherin expression was reversed when activation of ERK1/2 was blocked. Although EGF and TGFβ1 independently promoted migration of both oral keratinocytes and OSCC cells, EGF decreased TGFβ1-mediated migration of oral keratinocytes but enhanced migration of OSCC cells. Together, these data support a model wherein EGF signaling has an importantdoi:10.1242/jcs.021782 pmid:18544635 fatcat:vdnshdmeqfbxdfhxpu7tak4rbq