論文

査読有り 国際誌
2005年12月

Expression of SIP1 in oral squamous cell carcinomas: Implications for E-cadherin expression and tumor progression

International Journal of Oncology
  • Genta Maeda
  • ,
  • Tadashige Chiba
  • ,
  • Masahiro Okazaki
  • ,
  • Tazuko Satoh
  • ,
  • Yuji Taya
  • ,
  • Takaaki Aoba
  • ,
  • Koroku Kato
  • ,
  • Shuichi Kawashiri
  • ,
  • Kazushi Imai

27
6
開始ページ
1535
終了ページ
1541
記述言語
英語
掲載種別
研究論文(学術雑誌)

Loss of E-cadherin expression allows carcinoma cells to liberate from the primary site and enhances invasion and metastasis. The genetic aberration of E-cadherin is a rare event in sporadic carcinomas, and transcription repressors are considered to take a central role in E-cadherin loss. However, expression of E-cadherin repressors is largely dependent on tissue and cell type. To identify the repressor expressed in oral squamous carcinomas, we compared the expression levels of E-cadherin and repressors by real-time RT-PCR. Among the repressors including SNAIL, SLUG, SJP1, E12 and E47, SIP1 was inversely correlated to E-cadherin (P<0.05). Chromatin immunoprecipitation showed that SIP1 specifically bound to the E-cadherin promoter region. SIP1 expression was immunohistochemically detected in 27.7% of 47 oral carcinomas, and SIPl-positive carcinomas did not express E-cadherin (P<0.01). Thirteen patients with SIP1 staining showed a lower disease specific survival rate (P<0.05). Multivariate risk factor analysis demonstrated that SIP1 expression was an independent prognostic value for disease-specific overall survival (P<0.05). These results suggest that SIP1 contributes to the loss of E-cadherin expression and that detection of SIP1 expression is a predictive and prognostic tool in clinical management of oral carcinomas.

リンク情報
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/16273209
Scopus
https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=33644821962&origin=inward
Scopus Citedby
https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=33644821962&origin=inward
ID情報
  • ISSN : 1019-6439
  • eISSN : 1791-2423
  • PubMed ID : 16273209
  • SCOPUS ID : 33644821962

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