The LKB1 tumor suppressor kinase in human disease

被引：92

作者：

Katajisto, Pekka ^{[1
]}

Vallenius, Tea ^{[1
]}

Vaahtomeri, Kari ^{[1
]}

Ekman, Niklas ^{[1
]}

Udd, Lina ^{[1
]}

Tiainen, Marianne ^{[1
]}

Makela, Tomi P. ^{[1
]}

机构：

[1] Biomed Helsinki, Mol Canc Biol Program, Translat Genome Scale Biol & Inst Biomed, Helsinki 00014, Finland

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2007年 / 1775卷 / 01期

基金：

芬兰科学院;

关键词：

Peutz-Jeghers syndrome; LKB1; polyp; cancer; energy metabolism; polarity; lung adenocarcinoma; kinase;

D O I：

10.1016/j.bbcan.2006.08.003

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：

Inactivating germline mutations in the LKB1 gene underlie Peutz-Jeghers syndrome characterized by hamartomatous polyps and an elevated risk for cancer. Recent studies suggest the involvement of LKB1 also in more common human disorders including diabetes and in a significant fraction of lung adenocarcinomas. These observations have increased the interest towards signaling pathways of this turner suppressor kinase. The recent breakthroughs in understanding the molecular functions of the LKB1 indicate its contribution as a regulator of cell polarity, energy metabolism and cell proliferation. Here we review how the substrates and cellular functions of LKB1 may be linked to Peutz-Jeghers syndrome and other diseases, and discuss how some of the molecular changes associated with altered LKB1 signaling might be used in therapeutic approaches. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：63 / 75

页数：13

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