Summary: | 碩士 === 慈濟大學 === 分子生物及細胞生物研究所 === 96 === Claudins are the main tight junctional proteins and play a paracellular transport barrier to maintain tissue homeostasis and cellular polarity. Recently, aberrant expression of claudins are demonstrated in various tumors, however, the biological functions are still largely unknown. By systemic analysis, here, we reported an elevated expression of claudin-1 in nasopharyngeal carcinoma cells (NPC) in respond to apoptotic insults including serum deprivation and fluorouracil (5-FU) treatment. Of particular interest, the increased expression of claudin-1 apparently conferred persistent cell growth via against cells apoptosis. Intriguingly, epithelial-mesenchymal transition (EMT) process potentially promoted the aforementioned feature of claudin-1. Noteworthily, the dominant nuclear localization of claudin-1 was revealed, but irrelevant to its’ function. Furthermore, up-regulation and anti-apoptotic ability of claudin-1 also unrelated to outside-in induction and Akt or I�羠 pathways activation. In conclusion, our data not only showed an anti-apoptosis activity of claudin-1 in NPC cells growing, but also illustrated a novel regulatory pathway on claudin-1’s function.
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