Elucidation of the mechanism underlying thyroid carcinogenesis by galectin-3 overexpression, Development of thyroid-specific galectin-3-transgenic mice

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Galectin-3, a beta-gatacloside-binding lectin, is constitutively overexpressed in thyroid carcinomas of fotlicular cellorigin, whereas neither normal thyroid tissue, benign thyroid adenomatous goiter, nor thyroid follicular adenoma express a detectable amount of galectin-3. Galectin-3 is presumed to be involved in the thyroid carcinogenesis, themechanism underlying which remains largely unknown. The present study aims to develop thyroid-specific galectin-3 transgenic mice in order to give an insight into the thyroid carcinogenesis by overexpression of galectin-3. To this end, we have used the thyroglobulin gene promoter to drive the thyroid folticular cell overexpression of galectin-3 in transgenic mice. The overexpressed galectin-3 is functionally active when driven in this fashion, because it has conferred malignant phenotype on rat normal thyroid follicular cells FRTL-5. FRTL-5 cells overexpressing galectin-3 shows an anchorage-independent growth, which is not observed in either vehicle control or wild type cells. Three transgenic lines have been finally established, all of which express a high level of galectin-3 in the thyroid. These transgenic lines are under breeding, and will be subject to the examination of the pathogenesis of thyroid malignancies in near future.