JNK1, a potential therapeutic target for hepatocellular carcinoma

被引：34
作者：
Chen, Fei [1 ]
Beezhold, Kevin [1 ]
Castranova, Vince [1 ]
机构：
[1] NIOSH, Lab Canc Signaling & Epigenet, Hlth Effects Lab Div, Pathol & Physiol Res Branch, Morgantown, WV 26505 USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2009年 / 1796卷 / 02期
关键词：
JNK1; HCC; Signature genes; ROS; Progenitor cells; Epigenetics; JUN NH2-TERMINAL KINASE; N-TERMINAL-KINASE; VIRUS X-PROTEIN; NECROSIS-FACTOR-ALPHA; C-JUN; GENE-EXPRESSION; OXIDATIVE STRESS; KAPPA-B; TUMOR SUPPRESSION; WNT/BETA-CATENIN;
D O I：
10.1016/j.bbcan.2009.06.005
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：
Hepatocellular carcinoma (HCC) is the third leading cause of cancer death worldwide. Despite tremendous efforts to diagnose and institute new treatment regimens, the prognosis is still extremely poor. Therefore, knowledge of the molecular mechanisms governing the initiation, maintenance and progression of HCC is urgently needed. Recently, several groups have attributed an important role for c-Jun N-terminal kinase 1 (JNK1) in the pathogenesis of human HCC and its close association with the expression of HCC signature genes. In this review the various associations between JNK1 and HCC are discussed with the hope that targeting this pivotal kinase may lead to novel therapeutic approaches for this fatal disease. Published by Elsevier B.V.
引用
收藏
页码：242 / 251
页数：10
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