Requirement of c-Jun NH2-Terminal Kinase for Ras-Initiated Tumor Formation

被引：82
作者：
Cellurale, Cristina
Sabio, Guadalupe
Kennedy, Norman J.
Das, Madhumita
Barlow, Marissa
Sandy, Peter [2 ,3 ,4 ]
Jacks, Tyler [2 ,3 ,4 ]
Davis, Roger J. [1 ]
机构：
[1] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Program Mol Med, Worcester, MA 01605 USA
[2] MIT, Howard Hughes Med Inst, Cambridge, MA 02139 USA
[3] MIT, Dept Biol, Cambridge, MA 02139 USA
[4] MIT, Koch Inst Integrat Canc Res, Cambridge, MA 02139 USA
来源：
MOLECULAR AND CELLULAR BIOLOGY | 2011年 / 31卷 / 07期
基金：
美国国家卫生研究院;
关键词：
SIGNAL-TRANSDUCTION PATHWAY; TRANSCRIPTION FACTOR SNAIL; E-CADHERIN; GLIOBLASTOMA CELLS; MAP KINASE; K-RAS; JNK; EXPRESSION; CANCER; MICE;
D O I：
10.1128/MCB.01122-10
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The c-Jun NH2-terminal kinase (JNK) signal transduction pathway causes increased gene expression mediated, in part, by members of the activating transcription factor protein (AP1) group. JNK is therefore implicated in the regulation of cell growth and cancer. To test the role of JNK in Ras-induced tumor formation, we examined the effect of compound ablation of the ubiquitously expressed genes Jnk1 plus Jnk2. We report that JNK is required for Ras-induced transformation of p53-deficient primary cells in vitro. Moreover, JNK is required for lung tumor development caused by mutational activation of the endogenous KRas gene in vivo. Together, these data establish that JNK plays a key role in Ras-induced tumorigenesis.
引用
收藏
页码：1565 / 1576
页数：12
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