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Expression of epithelial-mesenchymal transition regulators SNAI2 and TWIST1 in thyroid carcinomas

Darya Buehler1, Heather Hardin, Weihua Shan

  • 1Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, K4/436 Clinical Science Center, Madison, WI, USA.

Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc
|August 18, 2012
PubMed

Insights

Anaplastic thyroid carcinomas show high expression of SLUG (SNAI2) and TWIST1, key inducers of epithelial-mesenchymal transition, correlating with loss of E-cadherin (CDH1). This suggests EMT drives anaplastic thyroid cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pathology

Background:

  • Epithelial-mesenchymal transition (EMT) is crucial for epithelial tumor progression, invasion, and metastasis.
  • SLUG (SNAI2) and TWIST1 are key EMT inducers that repress E-cadherin (CDH1) expression in poorly differentiated cancers.
  • The role of SNAI2 and TWIST1 in human thyroid cancer progression, particularly in anaplastic thyroid carcinoma (ATC), requires further investigation.

Purpose of the Study:

  • To investigate the expression patterns of SNAI2, TWIST1, and CDH1 proteins in various human thyroid cancer types.
  • To determine the phenotypic association of SNAI2 and TWIST1 with CDH1 expression in thyroid malignancies.
  • To elucidate the potential role of EMT in the pathogenesis of anaplastic thyroid carcinoma.

Main Methods:

  • Immunohistochemistry was used to assess SNAI2, TWIST1, and CDH1 protein expression on a tissue microarray of normal thyroids, follicular adenomas, papillary thyroid carcinomas, follicular carcinomas, and anaplastic thyroid carcinomas.
  • Quantitative reverse transcription PCR (qRT-PCR) was employed to analyze mRNA expression levels of SNAI2, TWIST1, and CDH1 in thyroid cell lines.
  • Findings were validated using whole tissue sections and an independent set of ATCs.

Main Results:

  • Anaplastic thyroid carcinomas exhibited strong nuclear SNAI2 (8/10 cases) and TWIST1 (5/10 cases) expression, frequently associated with absent CDH1.
  • In contrast, normal thyroid tissues, follicular adenomas, papillary, and follicular carcinomas were negative for SNAI2 and TWIST1 but showed strong CDH1 expression.
  • Thyroid cell line analysis revealed higher SNAI2 and TWIST1 mRNA in ATC lines, while normal thyroid cells had the highest CDH1 mRNA levels.

Conclusions:

  • The study supports a significant role for epithelial-mesenchymal transition in the development and progression of anaplastic thyroid carcinoma.
  • Elevated SNAI2 and TWIST1 expression, coupled with reduced CDH1, are characteristic features of anaplastic thyroid carcinoma.
  • These findings highlight SNAI2 and TWIST1 as potential biomarkers and therapeutic targets in anaplastic thyroid cancer.

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