doi: 10.5732/cjc.013.10086

Dysregulation of mTOR activity through LKB1 inactivation

Wei Zhou, Adam I. Marcus, Paula M. Vertino

The Winship Cancer Institute, Department of Hematology and Oncology, Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.

[Abstract] 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.

Chinese Journal of Cancer 2013, Volume: 32, Issue 8, Page: 427-433

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Wei Zhou, Adam I. Marcus, Paula M. Vertino. Dysregulation of mTOR activity through LKB1 inactivation . Chin J Cancer. 2013, 32(8):427-433. doi:10.5732/cjc.013.10086


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