Dysregulation of mTOR activity through LKB1 inactivation / 癌症
Chinese Journal of Cancer
;
(12): 427-433, 2013.
Artigo
em Inglês
| WPRIM
| ID: wpr-320585
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Adenocarcinoma
/
Transdução de Sinais
/
Neoplasias do Endométrio
/
Proteínas Serina-Treonina Quinases
/
Fosfatidilinositol 3-Quinases
/
Sirolimo
/
Proteínas Supressoras de Tumor
/
Usos Terapêuticos
/
Complexos Multiproteicos
/
Modelos Animais de Doenças
Limite:
Animais
/
Feminino
/
Humanos
Idioma:
Inglês
Revista:
Chinese Journal of Cancer
Ano de publicação:
2013
Tipo de documento:
Artigo
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