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Upregulated claudin‐1 expression confers resistance to cell death of nasopharyngeal carcinoma cells
Author(s) -
Lee JengWoei,
Hsiao WeiTing,
Chen HsiaYun,
Hsu LeePing,
Chen PeirRong,
Lin MingDer,
Chiu ShuJun,
Shih WenLing,
Hsu YihChih
Publication year - 2009
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.24857
Subject(s) - claudin , nasopharyngeal carcinoma , downregulation and upregulation , carcinogenesis , cancer research , apoptosis , tight junction , cell culture , biology , cadherin , cytoplasm , cell growth , protein kinase b , microbiology and biotechnology , cell , signal transduction , medicine , cancer , gene , genetics , radiation therapy
Accumulating evidence reveals that aberrant expression of claudins manifests in various tumors; however, their biological functions are poorly understood. Here, we report on the elevated expression of claudin‐1 in nasopharyngeal carcinoma (NPC) cell lines under serum deprivation or fluorouracil (5‐FU) treatment. Interestingly, an increase in expression of claudin‐1 considerably reduced apoptosis rather than enhancing cell proliferation. However, claudin‐1 expression and activity were unaffected by external stimuli or Akt and NF‐κB activation. Notably, predominant cytoplasmic and nuclear localization of claudin‐1 in NPC cells reflected the aforementioned feature. On the other hand, loss of epithelial morphology and E‐cadherin expression was associated with serum withdrawal in NPC cells. Interestingly, restoration of E‐cadherin inhibited the protein elevation and antiapoptotic activity of claudin‐1. In conclusion, our data demonstrate the regulation and novel biological function of claudin‐1 and indicate the important role of claudin‐1 in NPC tumorigenesis.