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Título : Snail family transcription factors are implicated in thyroid carcinogenesis.
Autor : Hardy, R. G.; Vicente-Dueñas, Carolina; González-Herrero, Inés; Flores, Teresa; Hughes, S.; Ross, J. A.; Sánchez García, Isidro; Tselepis, C.
Fecha de publicación : 2007
Citación : Am J Pathol. 2007 Sep;171(3):1037-46.
Resumen: E-Cadherin (CDH1) expression is reduced in thyroid carcinomas by primarily unknown mechanisms. In several tissues, SNAIL (SNAI1) and SLUG (SNAI2) 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 SNAI1 expression induces epithelial and mesenchymal mouse tumors. SNAI1, SNAI2, and CDH1 expression were analyzed in thyroidderived cell lines and samples of human follicular and papillary thyroid carcinoma by reverse transcriptasepolymerase chain reaction, Western blotting, and immunohistochemistry. The effect of SNAI1 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 SNAI1 levels are up-regulated. SNAI1 and SNAI2 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. SNAI1 expression in ori-3 cells repressed CDH1 transcription. Combi-TA mice developed papillary thyroid carcinomas, the incidence of which was increased by concomitant radiotherapy. In conclusion, SNAI1 and SNAI2 are ectopically expressed in thyroid carcinomas, and aberrant expression in mice is associated with papillary carcinoma development.
Descripción : Final full-text versión of the paper available at: http://dx.doi.org/10.2353/ajpath.2007.061211
URI : http://hdl.handle.net/10261/6253
DOI: 10.2353/ajpath.2007.061211
ISSN: 0002-9440
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