Snail family transcription factors are implicated in thyroid carcinogenesis

Research output: Contribution to journalArticle

Authors

  • RG Hardy
  • C Vicente-Duenas
  • I Gonzalez-Herrero
  • C Anderson
  • T Flores
  • JA Ross
  • I Sanchez-Garcia

Colleges, School and Institutes

Abstract

E-Cadherin (CDH1) expression is reduced in thyroid carcinomas by primarily unknown mechanisms. in several tissues, SNAIL (SNAI1) and SLUG (SNA12) induce epithelial-mesenchymal transition by altering target gene transcription, including CDH1 repression, but these transcription factors have not been studied in thyroid carcinoma. Recently, our group has provided direct evidence that ectopic SNAII expression induces epithelial and mesenchymal mouse tumors. SNAII, SNAI2, and CDH1 expression were analyzed in thyroid-derived cell lines and samples of human follicular and papillary thyroid carcinoma by reverse transcriptase-polymerase chain reaction, Western blotting, and immunchistochemistry. The effect of SNAII expression on CDH1 transcription was analyzed by reverse transcriptase-polymerase chain reaction and Western blotting in ori-3 cells. Thyroid carcinoma development was analyzed in CombitTA-Snail mice, in which SNAII levels are up-regulated. SNAII and SNA12 were not expressed in cells derived from normal thyroid tissue, or in normal human thyroid samples, but were highly expressed in cell lines derived from thyroid carcinomas, in human thyroid carcinoma samples, and their metastases. SNAII expression in ori-3 cells repressed CDR1 transcription. Combi-TA mice developed papillary thyroid carcinomas, the incidence of which was increased by concomitant radiotherapy. in conclusion, SNAII and SNA12 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is associated with papillary carcinoma development.

Details

Original languageEnglish
Pages (from-to)1037-1046
Number of pages10
JournalThe American Journal of Pathology
Volume171
Issue number3
Publication statusPublished - 1 Sep 2007