Loss of TSC1/TSC2 complex promotes cell migration through up-regulation of AKT2
作者单位：中国医学科学院基础医学研究所
会议名称：《第三届细胞结构与功能的信号基础研讨会》
会议日期：2010年
学科分类：0710[理学-生物学] 07[理学] 071009[理学-细胞生物学] 09[农学] 0901[农学-作物学] 090102[农学-作物遗传育种]
关 键 词：TSC1/TSC2 mTOR AKT2 cell migration
摘 要：Tuberous sclerosis complex.(TSC) is an autosomal dominant tumor disorder caused by inactive mutations of either TSC1 or TSC2 tumor ***1 and TSC2 form a protein complex in restraining the activity of mTOR and loss of this protein complex leads to hyperactive mTOR,resulting in uncontrolled cell growth and *** found that AKT2 was significantly increased in TSC2 mouse embryonic fibroblasts(MEFs),compared to TSC2 *** addition,kidney tumor tissues from Tsc2 heterozygous knockout mice also exhibited enhanced AKT2 ***,the elevated AKT2 expression was reversed by rapamycin,a mTOR ***,shRNA-mediated down-regulation of AKT2 expression in Tsc2 MEFs led to markedly reduced cell migration,as measured by wound healing and transwell migration *** conclude that TSCl/TSC2-mTOR pathway regulates cell migration through AKT2 and suggest that AKT2 may be a potential target for the treatment of TSC.