The LKB1 complex-AMPK pathway: the tree that hides the forest

被引:27
作者
Sebbagh, Michael [1 ,2 ,3 ]
Olschwang, Sylviane [1 ,2 ,3 ]
Santoni, Marie-Josee [1 ,2 ,3 ]
Borg, Jean-Paul [1 ,2 ,3 ]
机构
[1] INSERM, Ctr Rech Cancerol Marseille, F-13009 Marseille, France
[2] Inst J Paoli I Calmettes, F-13009 Marseille, France
[3] Univ Aix Marseille 2, F-13007 Marseille, France
关键词
Peutz-Jeghers syndrome; Lkb1; Regulation; AMPK-related kinases; Cell polarity; PEUTZ-JEGHERS-SYNDROME; ACTIVATED PROTEIN-KINASE; TUMOR-SUPPRESSOR LKB1; INTESTINAL EPITHELIAL-CELLS; GROWTH ARREST; LKB1-STRAD-MO25; COMPLEX; LKB1/STK11; GENE; CANCER SYNDROME; SPLICE VARIANT; CYCLE ARREST;
D O I
10.1007/s10689-011-9457-7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Initially identified as the Caenorhabditis elegans PAR-4 homologue, the serine threonine kinase LKB1 is conserved throughout evolution and ubiquitously expressed. In humans, LKB1 is causally linked to the Peutz-Jeghers syndrome and is one of the most commonly mutated genes in several cancers like lung and cervical carcinomas. These observations have led to classify LKB1 as tumour suppressor gene. Although, considerable dark zones remain, an impressive leap in the understanding of LKB1 functions has been done during the last decade. Role of LKB1 as a major actor of the AMPK/mTOR pathway connecting cellular metabolism, cell growth and tumorigenesis has been extensively studied probably to the detriment of other functions of equal importance. This review will discuss about LKB1 activity regulation, its effectors and clues on their involvement in cell polarity.
引用
收藏
页码:415 / 424
页数:10
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