Dysregulation of mTOR activity through LKB1 inactivation

被引：29

作者：

Zhou, Wei ^{[1
,2
,3
]}

Marcus, Adam I. ^{[1
,2
]}

Vertino, Paula M. ^{[1
,4
]}

机构：

[1] Emory Univ, Winship Canc Inst, Sch Med, Atlanta, GA 30322 USA

[2] Emory Univ, Sch Med, Dept Hematol & Oncol, Atlanta, GA 30322 USA

[3] Emory Univ, Sch Med, Dept Pathol & Lab Med, Atlanta, GA 30322 USA

[4] Emory Univ, Sch Med, Dept Radiat Oncol, Atlanta, GA 30322 USA

来源：

CHINESE JOURNAL OF CANCER | 2013年 / 32卷 / 08期

关键词：

Energetic stress; metabolism; bi-allelic inactivation; protein translation; PEUTZ-JEGHERS-SYNDROME; ACTIVATED PROTEIN-KINASE; LUNG-CANCER PROGRESSION; TUMOR-SUPPRESSOR LKB1; SOMATIC MUTATIONS; HOMOZYGOUS DELETION; PTEN/MMAC1; GENE; INCREASED RISK; CELL POLARITY; MOUSE MODEL;

D O I：

10.5732/cjc.013.10086

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

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.

引用

页码：427 / 433

页数：7

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