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

Research Project

Project/Area Number 13671777
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Otorhinolaryngology
Research InstitutionOsaka University

Principal Investigator

INOHARA Hidenori  Osaka University Graduate School of Medicine, Lecturer, 医学系研究科, 講師 (00273657)

Co-Investigator(Kenkyū-buntansha) AKAHANI Shiro  Osaka University Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (80322189)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2001: ¥1,300,000 (Direct Cost: ¥1,300,000)
Keywordsgalectin-3 / thyroid cancer / throglobulin promoter / transgcnic mice
Research Abstract

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.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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