| Summary: | 碩士 === 中國醫藥大學 === 醫學檢驗生物技術學系碩士班 === 101 === Thrombomodulin (TM), a calcium-dependent cell-cell adhesion molecule, is expressed in human keratinocytes and served as a differential biomarker for the clinical stages of skin cancers. Our previous study show that TM knockdown can induced lamellipodia formation, the proteomic analysis identified the interacting partners of TM including α-tubulin, β-tubulin, actin and ITSN. We also provided that TM regulats actin cytoskeleton via interaction with ITSN. Since TM is comparable to E-cadherin in adhesion and
morphoregulatory activities and ITSN is a modular scaffolding protein regulating the formation of endocytotic vesicles. We hypothesized that the TM may modulate the assembly of E-cadherin junctions by interplay with ITSN. Our results showed that si -RNA knockdown TM or ITSN increased the endocytosis of E-cadherin in HaCaT cells. The knockdown of TM or ITSN increased the lamellipodia formation whereas delayed the E-cadherin junction rebuilding by calcium switch assay. This implies that TM and ITSN play a role in forming E-cadherin-based adherens junctions. Besides, HaCaT cells downregulation of TM or ITSN were poorly differentiation by using organotypic cultures assay. These results suggest that TM and ITSN could modulate the functional of E-cadherin-mediated cell-cell adhesion and epithelial differentiation.
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