Oral Oncology
Volume 37, Issue 1 , Pages 65-71, January 2001

Reverse correlation of E-cadherin and snail expression in oral squamous cell carcinoma cells in vitro

First Department of Oral and Maxillofacial Surgery, School of Dentistry, University of Tokushima, Tokushima, Japan

Received 3 May 2000; accepted 17 May 2000.

Abstract 

The loss of E-cadherin expression has been shown to correlate to the invasion and metastasis of many types of carcinomas. We established E-cadherin positive (HOC719-PE) and negative (HOC719-NE) clones from an oral squamous cell carcinoma (SCC). HOC719-PE cells showed epithelial morphology with E-cadherin expression in the cell membrane, whereas HOC719-NE cells demonstrated fibroblastic morphology without E-cadherin expression. In invasion assay and three dimensional culture, HOC719-NE showed much higher invasive ability than HOC719-PE cells. These cells expressed similar levels of mRNAs for α- and β-catenin. However, HOC719-NE cells, but not HOC719-PE cells, showed strong expression of snail, a transcription factor implicated in the differentiation of epithelial cells into mesenchymal phenotype. This reverse expression of snail and E-cadherin was further observed in other SCC cells including HOC313, and TSU cells that we previously reported to show no expression of E-cadherin protein. These results indicated that the expression of snail has a key role for the acquisition of more invasive and metastatic phenotypes of SCC and the clones we reported here will be useful tools for understanding the mechanism of the transition from epithelial to mesenchymal SCC cells.

Keywords:  SCC, Invasion, E-cadherin, Catenin, Snail

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

PII: S1368-8375(00)00059-2

Oral Oncology
Volume 37, Issue 1 , Pages 65-71, January 2001