REPO

Annual Reports of Misasa Medical Center, Okayama University volume73
2003-02-01 発行

食道痛細胞におけるWntのベータカテ二ンTCF経路の活性化の検討

Mizushima, Takaaki Kaken ID researchmap
Ochi, Koji
Emori, Yasuyuki
Tanioka, Hiroaki
Sawa, Kiminari
Fujioka, Shinichi
Shinji, Toshiyuki
Koide, Norio
Tanizaki, Yoshiro
Publication Date
2003-02-01
Abstract
Although, accumulation of nuclear and cytoplasmic beta-catenin has been observed in ESCCs, mutation of APC and beta-catenin are not found in ESCCs. Therefore, another mechanism for cytoplasmic beta- catenin accumulation might exist in ESCCs. Materials and Methods: Human ESCCs cell lines and the 293 stable transfectants expressing Wnt-1, Wnt-5A, and Wnt-7A were cultured under standard conditions. The TOPFlash or FOPFlash reporter plasmids were transfected. Results: Transfected mutant beta-catenin as well as an axin fragment harbing the GSK3 beta interaction domain, the latter a potent GSK3 beta inhibitor. both robustly activated pTOPFlash in ESCCs cells. When pTOPFlash/pFOPFlash reporters were transfected in ESCCs cell lines followed by cocultivation with 293 cells that stably express Wnt -1, all cell lines except one demonstrated TCF mediated transcriptional. But, cells were co- cultured, Wnt - 7A or Wnt - 5A did not activate TCF mediated transcription in a cell number dependent fashion. Discussion; We report the activation of TCF promoter gene by extemal Wnt stimuli in ESCCs cells.
Keywords
esophageal carcinoma
Wnt
TCF
beta-catenin
ISSN
1348-1258
NCID
AA11840279
NAID