Dysregulation of mTOR activity through LKB1 inactivation

作     者：Wei Zhou Adam I. M arcus Paula M. Vertino 

作者机构：The Winship Cancer Institute Emory University School of Medicine Department of Hematology and Oncology Emory University School of Medicine Department of Pathology and Laboratory Medicine Emory University School of Medicine Department of Radiation Oncology Emory University School of Medicine 

出 版 物：《Chinese Journal of Cancer》 (Chinese Journal of Cancer)

年 卷 期：2013年第32卷第8期

页      面：427-433页

核心收录：

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

基　　金：supported by NIH Grant R01-CA140571 (to W.Z.) P01-CA116676 (to W.Z. and P.V.). W.Z. is an Anise McDaniel BrockScholar, Georgia Cancer Coalition Scholar, and American Cancer Research Scholar 

主　　题：mTOR 基因激活 丝氨酸 苏氨酸激酶 失活 失调 活性 信号转导通路 雷帕霉素 

摘      要：Mammalian target of rapamycin (mTOR) is aberrantly activated in many cancer types, and two rapamycin derivatives are currently approved by the Food and Drug Administration (FDA) of the United States for treating renal cell carcinoma. Mechanistically, mTOR is hyperactivated in human cancers either due to the genetic activation of its upstream activating signaling pathways or the genetic inactivation of its negative regulators. The tumor suppressor liver kinase B1 (LKB1), also known as serine/threonine kinase 11 (STK11), is involved in cell polarity, cell detachment and adhesion, tumor metastasis, and energetic stress response. A key role of LKB1 is to negatively regulate the activity of mTOR complex 1 (mTORC1). This review summarizes the molecular basis of this negative interaction and recent research progress in this area.