MYC activity mitigates response to rapamycin in prostate cancer through 4EBP1-mediated inhibition of autophagy.
Autophagy
; 6(2): 281-2, 2010 Feb.
Article
en En
| MEDLINE
| ID: mdl-20026909
ABSTRACT
Cancer cells have evolved exquisitely to ignore both intrinsic and extrinsic cell death signals, and resistance to cell death is a critical challenge facing clinical oncology. Autophagy, the catabolic recycling process that involves the fusion of autophagosomes containing sequestered cargo with lysosomes, has an enigmatic role in tumorigenesis. In times of metabolic stress due to deprived nutrition or hypoxia, tumor cells use autophagy as a scavenging mechanism for maintenance of critical processes and survival. However, modulation of the extent of autophagy plays a critical role, as excessive autophagy can result in a nonapoptotic and non-necrotic cell death (sometimes referred to as Type II programmed cell death). It is likely that the genetic context of specific cancers will have an impact upon whether autophagy is primarily a mechanism for survival or cell death.
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Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
6_ODS3_enfermedades_notrasmisibles
Problema de salud:
6_prostate_cancer
Asunto principal:
Fosfoproteínas
/
Neoplasias de la Próstata
/
Autofagia
/
Proteínas Proto-Oncogénicas c-myc
/
Sirolimus
/
Proteínas Adaptadoras Transductoras de Señales
/
Antibióticos Antineoplásicos
Límite:
Humans
/
Male
Idioma:
En
Revista:
Autophagy
Año:
2010
Tipo del documento:
Article
País de afiliación:
Estados Unidos