Inserm, U891, Centre de Recherche en Cancérologie de Marseille, 27 Blv Lei Roure, 13009, Marseille, France.
Fam Cancer. 2011 Sep;10(3):415-24. doi: 10.1007/s10689-011-9457-7.
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.
最初被鉴定为秀丽隐杆线虫 PAR-4 同源物的丝氨酸苏氨酸激酶 LKB1 在进化过程中是保守的,并且广泛表达。在人类中,LKB1 与 Peutz-Jeghers 综合征有关,并且是几种癌症(如肺癌和宫颈癌)中最常突变的基因之一。这些观察结果导致将 LKB1 归类为肿瘤抑制基因。尽管仍然存在相当大的未知领域,但在过去十年中,对 LKB1 功能的理解取得了令人瞩目的飞跃。LKB1 作为连接细胞代谢、细胞生长和肿瘤发生的 AMPK/mTOR 途径的主要因子的作用已被广泛研究,这可能是因为其他同等重要的功能受到了损害。这篇综述将讨论 LKB1 的活性调节、其效应物以及它们在细胞极性中的参与的线索。