| Summary: | 碩士 === 慈濟大學 === 生命科學系碩士班 === 105 === Claudin superfamily has been demonstrated an important role in cell to cell communication. Of interest, numerous evidences reveal that abnormal expression of claudins, such as claudin-1 contributed to tumor progression. Previous study demonstrated claudin-1 expression confers resistance to cell death of nasopharyngeal carcinoma (NPC) cells. However, the mechanism is still not clear. In this study, exogenous expression of claudin-1 in NPC cells was utilized to assess effect of claudin-1 in tumor cells. Via anchorage independent assay and 3-D tumor spheroid formation analysis, intriguingly, overexpressed claudin-1 not only reduced tumor cells colonies size, but repressed the cell cell’s connection. Base on the change of the cell’s connection, we examine the cell differentiation marker Cytokeratin 8(CK8), than found the CK8 upregulated in two Claudin-1 stable expressing clones. Thus, our preliminary results show that claudin-1 reduced tumor cells colonies size of NPC.
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