Expression of the cadherin-catenin complex in well-differentiated human thyroid neoplastic tissue

Shih Horng Huang, Jiahn Chun Wu, King Jen Chang, Koung Yi Liaw, Seu Mei Wang*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

E-cadherin is a member of the cadherin family that plays a major role in epithelial integrity and tumorigenesis. Catenins are a group of cytoplasmic proteins that regulate the intracellular anchorage of cadherin and are required for the linkage between cadherin and the actin cytoskeleton. Loss of E-cadherin contributes to the pathogenesis in tumor invasion and gives a poor prognosis. In order to investigate the adhesion property of intercellular junctions in thyroid tumors, expression of α- β-, and γ-catenin should also be studied. A correlation between these molecular markers and malignancy would be useful as a preoperative diagnostic test for thyroid neoplasms. The expression of E-cadherin, α-, β-, and γ-catenin were studied in normal and neoplastic thyroid tissue by immunofluorescence microscopy and Western blot analysis. In the normal thyroid and in nodular goiter, and follicular adenoma, staining for E-cadherin, α-, β-, and γ-catenin was seen mainly at the lateral surface of epithelial cells in the follicle and the presence of these molecules was confirmed by Western blot analysis. Follicular carcinoma tissue stained positive for E-cadherin and α-catenin, but the results of β- and γ-catenin immunostaining were highly variable, with β-catenin being absent in most follicular carcinomas (8/10) and γ-catenin being absent in some follicular carcinomas (3/10). These results suggest that E-cadherin expression was not reduced during the pathogenesis of differentiated thyroid malignancies. Impairment of the cadherin-catenin complex at the cell junction may contribute to the malignant progression of differentiated thyroid neoplastic tissue.

Original languageEnglish
Pages (from-to)1095-1103
Number of pages9
JournalThyroid
Volume9
Issue number11
DOIs
StatePublished - Nov 1999

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