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Anoxia/reoxygenation down-regulates the expression of E-cadherin in human colon cancer cell lines.

Abstract
The E-cadherin-mediated cell-cell adhesiveness is a critical factor for carcinoma cell invasion and metastasis. Anoxia/reoxygenation is known to occur in cancer tissues. In this study, we investigated whether anoxia/reoxygenation induces the down-regulation of E-cadherin expression in the human colon cancer cell lines HT-29, and SW1116. Colon cancer cells were exposed to anoxia (2 h) followed by reoxygenation (4-46 h). The subsequent expression of E-cadherin on the cell surface was examined by immunocytochemistry and enzyme-linked immunosorbent assays, the total amount of E-cadherin protein was examined by Western blotting, and the E-cadherin mRNA level was examined by a real-time polymerase chain reaction assay. The expression of E-cadherin on the cell surface and the total amount of E-cadherin protein were transiently reduced after anoxia/reoxygenation. On the other hand, the E-cadherin mRNA level was not decreased during reoxygenation. Pretreatment with actinomycin D or reagents that interfere with the activation of NF-kappaB significantly attenuated the down-regulation of E-cadherin, which implicated a role for the de novo protein synthesis. These results indicate that anoxia/reoxygenation induces a transient reduction of E-cadherin expression in human colon cancer cells through NF-kappaB dependent transcriptional pathway.
AuthorsSatoshi Kokura, Norimasa Yoshida, Eiko Imamoto, Miho Ueda, Takeshi Ishikawa, Kazuhiko Uchiyama, Masashi Kuchide, Yuji Naito, Takeshi Okanoue, Toshikazu Yoshikawa
JournalCancer letters (Cancer Lett) Vol. 211 Issue 1 Pg. 79-87 (Jul 28 2004) ISSN: 0304-3835 [Print] Ireland
PMID15194219 (Publication Type: Journal Article)
CopyrightCopyright 2004 Elsevier Ireland Ltd.
Chemical References
  • Cadherins
  • Dactinomycin
  • Oxygen
Topics
  • Cadherins (genetics, metabolism)
  • Cell Hypoxia (genetics)
  • Cell Line, Tumor
  • Colonic Neoplasms (metabolism, pathology)
  • Dactinomycin (pharmacology)
  • Down-Regulation
  • HT29 Cells
  • Humans
  • Oxygen (metabolism)
  • Transcription, Genetic

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