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Snail family transcription factors are implicated in thyroid carcinogenesis

Robert G Hardy1, Carolina Vicente-Dueñas, Ines González-Herrero

  • 1Tissue Injury and Repair Group, Centre for Regenerative Medicine, University of Edinburgh, Division of Clinical and Surgical Sciences, Room FU501, Chancellors Bldg, 49 Little France Crescent, Edinburgh EH16 4SB, UK. r.hardy@ed.ac.uk

The American Journal of Pathology
|August 29, 2007
PubMed

Insights

SNAIL (SNAI1) and SLUG (SNAI2) are highly expressed in thyroid carcinomas, repressing E-Cadherin (CDH1) and promoting tumor development. Aberrant expression in mice also led to papillary thyroid carcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • E-Cadherin (CDH1) expression reduction in thyroid carcinomas is poorly understood.
  • SNAIL (SNAI1) and SLUG (SNAI2) are known inducers of epithelial-mesenchymal transition and CDH1 repression in other tissues.
  • Previous studies showed ectopic SNAI1 induces epithelial and mesenchymal tumors in mice.

Purpose of the Study:

  • To investigate the role of SNAI1 and SNAI2 in thyroid carcinoma development.
  • To analyze the expression of SNAI1, SNAI2, and CDH1 in thyroid cancer cell lines and human samples.
  • To determine the effect of SNAI1 on CDH1 transcription and its role in tumor formation in a mouse model.

Main Methods:

  • Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to analyze gene and protein expression.
  • Immunohistochemistry was performed on human thyroid carcinoma samples.
  • A transgenic mouse model (CombitTA-Snail) was used to study tumor development with SNAI1 up-regulation.

Main Results:

  • SNAI1 and SNAI2 were not expressed in normal thyroid tissues but were highly expressed in thyroid carcinoma cell lines, human tumors, and metastases.
  • SNAI1 expression repressed CDH1 transcription in ori-3 cells.
  • Combi-TA mice developed papillary thyroid carcinomas, with increased incidence following radiotherapy.

Conclusions:

  • SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas.
  • Aberrant SNAI1 and SNAI2 expression is linked to thyroid carcinoma development.
  • These findings suggest SNAI1 and SNAI2 as potential therapeutic targets in thyroid cancer.

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