CAJ | 학술논문

研究表明,甲状腺激素受体(TR)在许多肿瘤的发生过程中伴有染色体杂合子丢失、基因启动子区甲基化及基因突变等,出现TR mRNA或蛋白质表达异常,且TR异常与某些神经系统肿瘤如星形细胞瘤和垂体瘤的分化程度相关.目前,关于TR的作用途径及机制主要包括:垂体瘤转化-1、β-连环蛋白等肿瘤相关因子和细胞外信号调节激酶、磷脂酰肌醇-3激酶信号传导通路等.
연구표명,갑상선격소수체(TR)재허다종류적발생과정중반유염색체잡합자주실、기인계동자구갑기화급기인돌변등,출현TR mRNA혹단백질표체이상,차TR이상여모사신경계통종류여성형세포류화수체류적분화정도상관.목전,관우TR적작용도경급궤제주요포괄:수체류전화-1、β-련배단백등종류상관인자화세포외신호조절격매、린지선기순-3격매신호전도통로등.
Many studies demonstrate alterations in the level of mRNA or protein expression of thyroid hormone receptor (TR) which result from chromosomal loss of heterozygosity,methylation status of promoter region and mutation in different types of human cancers. Moreover,abnormity of TR has connection with differentiation of some neural tumors,such as astrocytomas and pituitary tumor. Pituitary tumor-transforming 1 and β-catenin have a great impact on the ways and the mechanism of the TR function as well as signal transduction pathways of extracellular signal-regulated kinase and phosphatidylinositol 3-kinase.