Expression of the Cadherin-Catenin Complex in Well-Differentiated Human Thyroid Neoplastic Tissue

Huang, Shih-Horng; Wu, Jen Leih; Chang, King‐Jen; Liaw, Koung-Yi; Wang, Seu‐Mei

doi:10.1089/thy.1999.9.1095

Cited by 27 publications

(15 citation statements)

References 16 publications

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“…These results have been supported by other workers, some of whom have also proposed E-cadherin expression as a prognostic indicator [8][9][10][11][12]. Additional studies suggest that while both differentiated [13][14][15] and poorly differentiated thyroid carcinomas [16] do express E-cadherin, it is relocated from the cell surface to the cytoplasm.…”

supporting

confidence: 74%

Real-time Quantitative Analysis of E-cadherin Expression in ret/PTC-1-Activated Thyroid Neoplasms

Smyth

Sheils²,

Finn

et al. 2001

Int J Surg Pathol

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Papillary thyroid carcinoma (PTC), the most common variety of thyroid cancer, is found in a variety of morphologic variants, usually grows slowly, and is clinically indolent, although rare, aggressive forms, with local invasion or distant metastases, occur. Our group has previously demonstrated an association between Hashimoto thyroiditis and ret/PTC-1 activation, and have hypothesised that c-ret activation might be implicated in immune reaction to thyroid epithelium. The objective of this study was to examine expression of the cellular adhesion molecule, E-cadherin, in various thyroid tumor types and Hashimoto thyroiditis in the context of ret/PTC-1 positivity by using laser capture microdissection and TaqMan reverse transcription-polymerase chain reaction (RT-PCR). Variable down-regulation of E-cadherin among carcinomas was demonstrated, with anaplastic carcinomas showing little or no expression. Follicular thyroid carcinomas consistently had significantly decreased E-cadherin expression compared with papillary thyroid carcinomas. The ret/PTC-1-positive papillary thyroid carcinoma (PTCret+) and Hashimoto thyroiditis cases had consistently lower E-cadherin expression levels than the corresponding ret/PTC-1-negative papillary carcinomas (PTCret-), suggesting not only an association between ret activation and the loss of cellular adhesion but also, more significantly, an association between papillary thyroid carcinoma and Hashimoto thyroiditis.

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supporting

confidence: 74%

Real-time Quantitative Analysis of E-cadherin Expression in ret/PTC-1-Activated Thyroid Neoplasms

Smyth

Sheils²,

Finn

et al. 2001

Int J Surg Pathol

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“…This is concordant with the reports by other authors [7,8,12,16,20,23,26,27]. Only von Wasilewski et al (1997) did not find differences in E-CAD expression between PTC and FTC [11].…”

Section: Discussionsupporting

confidence: 92%

E-cadherin expression is more associated with histopathological type of thyroid cancer than with the metastatic potential of tumors

Słowińska-Klencka¹,

Sporny²,

Stasikowska-Kanicka³

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The aim of this study was to evaluate the relationship between abnormal expression of E-cadherin (E-CAD) and the extracapsular extension of tumors, lymph node involvement and the presence of metastasis in various types of thyroid cancers. Histopathological specimens of 35 benign thyroid lesions and 122 malignant tumors (papillary, follicular, poorly differentiated and undifferentiated cancers) were analyzed. E-CAD immunostaining intensity, its subcellular localization, homogeneity within lesion, and the relation of staining intensity between tumor and surrounding thyroid parenchyma were evaluated. The obtained results show that the variants of differentiated cancers with a poorer prognosis (i.e. tall cell and follicular variants of papillary cancer and widely invasive follicular cancers) present reduced intensity of E-CAD expression, its abnormal localization or heterogeneity of staining more frequently than classical papillary cancers and minimally invasive follicular cancers. However, the assessment of E-CAD expression does not allow the prediction of extrathyroidal growth of thyroid cancers.

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“…Whereas the Pg-related b-catenin represents a potential oncogene, Pg appears to play a tumour suppressor role (33,39,40). Even though the contribution of dysregulated Pg expression to thyrocyte transformation and thyroid carcinoma progression is unknown at present, studies in differentiated and anaplastic thyroid carcinoma tissues (11,14,42) and in cell culture models (10,12,13) demonstrated frequent loss of Pg, in part along with de-differentiation. Mechanisms are mostly unknown so far and could include gene mutations/deletions, altered RNA or protein stability, hormonal dysregulation, loss/overexpression of transcriptional regulators and epigenetic silencing.…”

Section: Discussionmentioning

confidence: 99%

Molecular cloning of a functional promoter of the human plakoglobin gene

Pötter

Braun

Lehmann³

et al. 2001

European Journal of Endocrinology

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Objective: Plakoglobin (Pg) is the only cytoplasmic protein component common to both junctional complexes mediating cell±cell adhesion, adherens junctions and desmosomes. In these complexes Pg appears to act as a linker protein anchoring transmembrane proteins of the cadherin superfamily to the actin cytoskeleton and intermediate ®lament system respectively. Intercellular adhesion is frequently disturbed in skin diseases and in carcinomas, enabling tumour progression and metastasis. Whereas Pg expression is lost in some thyroid tumours and carcinoma cell lines, little information on Pg gene regulation is currently available owing to a lack of promoter studies. Design and methods: We have cloned and sequenced genomic DNA from a human library that resulted in 979 bp upstream of the published Pg cDNA. The transcriptional start was mapped by rapid ampli®cation of cDNA ends. Methylation-speci®c PCR of bisul®te-modi®ed cell line DNA was applied to probe the methylation status of a promoter-associated CpG island. Reporter-gene constructs of various promoter fragments were transiently transfected in thyroid carcinoma cell lines and their activities were determined by luciferase measurements. Results and conclusions: A 1 kb DNA fragment harbouring a functional promoter of the human Pg gene was cloned and characterized. The sequence lacks a canonical TATA box, but contains putative CCAAT boxes as well as various putative binding sites for transcription factors, among them SP1 and AP2, proximal to the transcriptional start. Considerable promoter activity was found in thyroid cell lines and deletion analysis indicated that a 300 bp region proximal to the 5 H -untranslated region of the mRNA represents the minimal promoter of the human Pg gene. As cells lacking endogenous Pg expression were found to contain methylated CpG dinucleotides in a CpG island located around the transcriptional start site, it is suggested that epigenetic mechanisms such as DNA methylation contribute to dysregulated Pg expression.

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Expression of the Cadherin-Catenin Complex in Well-Differentiated Human Thyroid Neoplastic Tissue

Cited by 27 publications

References 16 publications

Real-time Quantitative Analysis of E-cadherin Expression in ret/PTC-1-Activated Thyroid Neoplasms

Real-time Quantitative Analysis of E-cadherin Expression in ret/PTC-1-Activated Thyroid Neoplasms

E-cadherin expression is more associated with histopathological type of thyroid cancer than with the metastatic potential of tumors

Molecular cloning of a functional promoter of the human plakoglobin gene

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