論文

査読有り
2016年11月

Aberrant expression of the tight junction molecules claudin-1 and zonula occludens-1 mediates cell growth and invasion in oral squamous cell carcinoma

HUMAN PATHOLOGY
  • Hamzah Babkair
  • ,
  • Manabu Yamazaki
  • ,
  • Md. Shihab Uddin
  • ,
  • Satoshi Maruyama
  • ,
  • Tatsuya Abe
  • ,
  • Ahmed Essa
  • ,
  • Yoshimasa Sumita
  • ,
  • Md. Shahidul Ahsan
  • ,
  • Wael Swelam
  • ,
  • Jun Cheng
  • ,
  • Takashi Saku

57
開始ページ
51
終了ページ
60
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.humpath.2016.07.001
出版者・発行元
W B SAUNDERS CO-ELSEVIER INC

We reported that altered cell contact mediated by E-cadherin is an initial event in the pathogenesis of oral epithelial malignancies. To assess other effects of cell adhesion, we examined the expression levels of tight junction (TJ) molecules in oral carcinoma in situ (CIS) and squamous cell carcinoma (SCC). To identify changes in the expression of TJ molecules, we conducted an analysis of the immunohistochemical profiles of claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1) in surgical specimens acquired from patients with oral SCC containing foci of epithelial dysplasia or from patients with CIS. We used immunofluorescence, Western blotting, reverse-transcription polymerase chain reaction, and RNA interference to evaluate the functions of CLDN-1 and ZO-1 in cultured oral SCC cells. TJ molecules were not detected in normal oral epithelial tissues but were expressed in SCC/CIS cells. ZO-1 was localized within the nucleus of proliferating cells. When CLDN-1 expression was inhibited by transfecting cells with specific small interference RNAs, SCC cells dissociated, and their ability to proliferate and invade Matrigel was inhibited. In contrast, although RNA interference mediated inhibition of ZO-1 expression did not affect cell morphology, it inhibited cell proliferation and invasiveness. Our findings indicated that the detection of TJ molecules in the oral epithelia may serve as a marker for the malignant phenotype of cells in which CLDN-1 regulates proliferation and invasion. (C) 2016 Elsevier Inc. All rights reserved.


リンク情報
DOI
https://doi.org/10.1016/j.humpath.2016.07.001
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27436828
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000386644600009&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.humpath.2016.07.001
  • ISSN : 0046-8177
  • eISSN : 1532-8392
  • PubMed ID : 27436828
  • Web of Science ID : WOS:000386644600009

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