Analysis of molecular mechanism of tumor progression induced by an alpha6beta4 integrin

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In this study, to elucidate the role of N-glycosylation on β4 integrin, we established the keratinocytes re-expressing wild-type or N-glycosylation-defective β4 integrin in β4 integrin null keratinocytes. The analysis using the keratinocytes indicated that N-glycosylation plays important roles for integrin-mediated cell adhesion and migration. In addition, we found that β4 integrin forms supramolecular complex with EGFR through cross-linking with galectin-3-mediated N-glycans, thereby promoting cellular signaling and the following cellular function.