Oncogenic cooperation between H-Twist and N-Myc overrides failsafe programs in cancer cells.
Cancer Cell
; 6(6): 625-30, 2004 Dec.
Article
em En
| MEDLINE
| ID: mdl-15607966
ABSTRACT
N-Myc oncogene amplification is a frequent event in neuroblastoma and is strongly correlated with advanced disease stage and treatment failure. Similarly to c-Myc oncogenic activation, N-Myc deregulation promotes both cell proliferation and p53-dependent apoptosis by sensitizing cells to a variety of insults. Intriguingly, p53 mutations are uncommon in neuroblastomas, strongly suggesting that an alternative cooperating event circumvents this safeguard against oncogene-driven neoplasia. By performing a pangenomic cDNA microarray analysis, we demonstrate that human Twist is constantly overexpressed in N-Myc-amplified neuroblastomas. H-Twist overexpression is responsible for the inhibition of the ARF/p53 pathway involved in the Myc-dependent apoptotic response. This oncogenic cooperation of two key regulators of embryogenesis causes cell transformation and malignant outgrowth.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Fatores de Transcrição
/
Proteínas Nucleares
/
Transformação Celular Neoplásica
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Proteínas Proto-Oncogênicas c-myc
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Neuroblastoma
Idioma:
En
Ano de publicação:
2004
Tipo de documento:
Article