LKB1 tumor suppressor: Therapeutic opportunities knock when LKB1 is inactivated

作     者：Wei Zhou Jun Zhang Adam I.Marcus 

作者机构：Department of Hematology and Medical OncologyThe Winship Cancer InstituteEmory University School of MedicineAtlantaGeorgia 

出 版 物：《Genes & Diseases》 (基因与疾病（英文）)

年 卷 期：2014年第1卷第1期

页      面：64-74页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：This work was supported in part by R01-CA140571,P01 CA116676 Anise McDaniel Brock Scholar fund to WZ,1RO1CA142858 to A.M.,and P30CA138292 to Winship Cancer Institute 

主　　题：Metabolic stress Targeted therapy Tumor Suppressor Tumor vulnerability 

摘      要：LKB1 is commonly thought of as a tumor suppressor gene because its hereditary mutation is responsible for a cancer syndrome,and somatic inactivation of LKB1 is found in nonsmall cell lung cancer,melanoma,and cervical ***,unlike other tumor suppressors whose main function is to either suppress cell proliferation or promote cell death,one of the functions of LKB1-regulated AMPK signaling is to suppress cell proliferation in order to promote cell survival under energetic stress *** unique,pro-survival function of LKB1 has led to the discovery of reagents,such as phenformin,that specifically exploit the vulnerability of LKB1-null cells in their defect in sensing energetic *** targeted agents represent a novel treatment strategy because they induce cell killing when LKB1 is *** review article summarizes various vulnerabilities of LKB1-mutant cells that have been reported in the literature and discusses the potential of using existing or developing novel reagents to target cancer cells with defective LKB1.