dUev1a modulates TNF-JNK mediated tumor progression and cell death in Drosophila

被引：49

作者：

Ma, Xianjue ^{[1
]}

Yang, Lixia ^{[1
]}

Yang, Yang ^{[1
]}

Li, Maoquan ^{[1
]}

Li, Wenzhe ^{[1
]}

Xue, Lei ^{[1
]}

机构：

[1] Tongji Univ, Dept Intervent Radiol, Shanghai Key Lab Signaling & Dis Res, Shanghai Peoples Hosp 10,Sch Life Sci & Technol, Shanghai 200092, Peoples R China

来源：

DEVELOPMENTAL BIOLOGY | 2013年 / 380卷 / 02期

基金：

高等学校博士学科点专项科研基金; 中国国家自然科学基金;

关键词：

Cell death; dUev1a; Tumor invasion; JNK; TNF; UBIQUITIN-CONJUGATING ENZYMES; ONCOGENIC RAS; ACTIVATION; PATHWAY; PROTEIN; SUPERFAMILY; APOPTOSIS; BEHAVIOR; HOMOLOG; GROWTH;

D O I：

10.1016/j.ydbio.2013.05.013

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Loss of cell polarity cooperates with oncogenic Ras to induce JNK-dependent tumor growth and invasion. To identify additional genes that modulate tumor progression, we have performed a genetic screen in Drosophila and found that loss of dUev1a, the ortholog of mammalian Uev1, suppressed lgl(-/-)/Ras(V12) induced JNK-mediated tumor growth and invasion. Furthermore, loss of dUev1a suppressed TNF ortholog Eiger-induced JNK-mediated cell invasion and cell death. Finally, dUev1a cooperated with Bendless to activate JNK signaling through dTRAF2. Together, our data indicate that dUev1a encodes an essential component of the evolutionary conserved TNF-JNK signaling pathway that modulates tumor progression and cell death in metazoan. (c) 2013 Elsevier Inc. All rights reserved.

引用

页码：211 / 221

页数：11

共 43 条

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