JNK-Induced Apoptosis, Compensatory Growth, and Cancer Stem Cells

被引：187

作者：

Chen, Fei ^{[1
]}

机构：

[1] Wayne State Univ, Eugene Applebaum Coll Pharm & Hlth Sci, Dept Pharmaceut Sci, Detroit, MI 48201 USA

来源：

CANCER RESEARCH | 2012年 / 72卷 / 02期

关键词：

JUN NH2-TERMINAL KINASE; CONTROLS SELF-RENEWAL; NECROSIS-FACTOR-ALPHA; N-TERMINAL KINASE-1; LIVER-CANCER; HISTONE H3; GENE-EXPRESSION; IKK-BETA; KAPPA-B; DROSOPHILA;

D O I：

10.1158/0008-5472.CAN-11-1982

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Overwhelming evidence suggests that c-jun-NH2-kinases (JNK) are a set of key stress-responsive kinases that mediate cell apoptosis, which is an important process for tumor suppression. However, JNKs have also been implicated in the malignant transformation and tumorigenesis of cells. This review attempts to reconcile these 2 contradictory functions of JNKs with recent discoveries on the role of JNKs in compensatory growth of neighboring cells and stem cells, which may provide new mechanistic understanding about the role of JNKs in the regulation of cancer stem cells and the pathogenesis of cancers. Cancer Res; 72(2); 379-86. (C)2012 AACR.

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页码：379 / 386

页数：8

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