This Article Full Text Full Text (PDF) All Versions of this Article: jhc.6A6958.2006v1 54/11/1263    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Takkunen, M. Articles by Virtanen, I. Search for Related Content PubMed PubMed Citation Articles by Takkunen, M. Articles by Virtanen, I. Social Bookmarking                      What's this?

Snail-dependent and -independent Epithelial–Mesenchymal Transition in Oral Squamous Carcinoma Cells

Minna Takkunen, Reidar Grenman, Mika Hukkanen, Matti Korhonen, Antonio García de Herreros and Ismo Virtanen

Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland (MT,MH,IV); Department of Otorhinolaryngology, Head and Neck Surgery, Turku University Central Hospital, Turku, Finland (RG); Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland (MK); and Unitat de Biologia Cel.lular i Molecular, Institut Municipal d'Investigació Mèdica, Universitat Pompeu Fabra, Barcelona, Spain (AGH)

Correspondence to: Minna Takkunen, MD, Institute of Biomedicine/Anatomy, P.O. Box 63 (Haartmaninkatu 8), FI-00014 University of Helsinki, Helsinki, Finland. E-mail: minna.k.takkunen{at}helsinki.fi

Disappearance of E-cadherin is a milestone for epithelial–mesenchymal transition (EMT), found both in carcinomas and in some fibrotic diseases. We have studied the mechanisms of EMT in oral squamous cell carcinoma (SCC) cells isolated from primary tumor (43A) and its recurrent tumor (43B). Whereas the cells from primary carcinoma displayed a typical phenotype of squamous epithelial cells including E-cadherin and laminin-332 (laminin-5), cells from recurrent tumor expressed characteristics of dedifferentiated, EMT-experienced tumors. 43B cells expressed E-cadherin repressors ZEB-1/EF1 and especially ZEB-2/SIP1, which therefore appear as candidates for endogenous EMT in these cells. Differences between endogenous and exogenous EMT were assessed by transfecting 43A cells with SNAIL cDNA. SNAIL-transfected cells showed complete EMT phenotype with fibroblastoid appearance, vimentin filaments, E-cadherin/N-cadherin switch, lack of hemidesmosomes and, as a new feature of EMT, lack of laminin-332 synthesis. Upregulation of ZEB-1 and ZEB-2 was evident in these cells, suggesting that SNAIL can regulate these E-cadherin repressors. New monoclonal antibodies against SNAIL showed nuclear immunoreactivity not only in the SNAIL-transfected cells but also in carcinoma cells lacking production of Lm-332 and showing signs of EMT. These results suggest that changes in the epithelial cell differentiation program and EMT in SCC cells can result from the interplay among several E-cadherin repressors; however, SNAIL alone is able to accomplish a complete EMT. (J Histochem Cytochem 54:1263–1275, 2006)

Key Words: epithelial–mesenchymal transition • E-cadherin • ZEB-1 • ZEB-2 • SNAIL • laminin-332

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				Y Kabasawa, K Nagumo, Y Takeda, N Kawashima, N Okada, K Omura, A Yamaguchi, and K Katsube Amelogenin positive cells scattered in the interstitial component of odontogenic fibromas J. Clin. Pathol., July 1, 2008; 61(7): 851 - 855. [Abstract] [Full Text] [PDF]

Guidelines | Subscriptions | About | exPRESS - Current - Archive | Business Information | Contact

The Journal of Histochemistry & Cytochemistry is owned, published, and licensed by The Histochemical Society © 2006