A comparison of oncogene-induced senescence and replicative senescence: implications for tumor suppression and aging.
Age (Dordr)
; 36(3): 9637, 2014 Jun.
Article
en En
| MEDLINE
| ID: mdl-24647599
ABSTRACT
Cellular senescence is a stable proliferation arrest associated with an altered secretory pathway, the senescence-associated secretory phenotype. However, cellular senescence is initiated by diverse molecular triggers, such as activated oncogenes and shortened telomeres, and is associated with varied and complex physiological endpoints, such as tumor suppression and tissue aging. The extent to which distinct triggers activate divergent modes of senescence that might be associated with different physiological endpoints is largely unknown. To begin to address this, we performed gene expression profiling to compare the senescence programs associated with two different modes of senescence, oncogene-induced senescence (OIS) and replicative senescence (RS [in part caused by shortened telomeres]). While both OIS and RS are associated with many common changes in gene expression compared to control proliferating cells, they also exhibit substantial differences. These results are discussed in light of potential physiological consequences, tumor suppression and aging.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Oncogenes
/
Envejecimiento
/
ARN Neoplásico
/
Regulación Neoplásica de la Expresión Génica
/
Telómero
/
Senescencia Celular
/
Neoplasias
Límite:
Humans
Idioma:
En
Revista:
Age (Dordr)
Año:
2014
Tipo del documento:
Article
País de afiliación:
Reino Unido