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Chinese Journal of Cancer ; (12): 427-433, 2013.
Artigo em Inglês | WPRIM | ID: wpr-320585

RESUMO

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.


Assuntos
Animais , Feminino , Humanos , Proteínas Quinases Ativadas por AMP , Metabolismo , Adenocarcinoma , Tratamento Farmacológico , Metabolismo , Antibióticos Antineoplásicos , Usos Terapêuticos , Modelos Animais de Doenças , Neoplasias do Endométrio , Tratamento Farmacológico , Metabolismo , Alvo Mecanístico do Complexo 1 de Rapamicina , Complexos Multiproteicos , Metabolismo , Fosfatidilinositol 3-Quinases , Metabolismo , Proteínas Serina-Treonina Quinases , Metabolismo , Proteínas Proto-Oncogênicas c-akt , Metabolismo , Transdução de Sinais , Sirolimo , Usos Terapêuticos , Serina-Treonina Quinases TOR , Metabolismo , Proteínas Supressoras de Tumor , Metabolismo
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