Inhibitory Effect of Melanoma Differentiation Associated Gene-7/Interleukin-24 on Invasion In Vitro of Human Melanoma Cancer Cells
Journal of Korean Medical Science
; : 833-839, 2013.
Article
em En
| WPRIM
| ID: wpr-159658
Biblioteca responsável:
WPRO
ABSTRACT
The acquisition of metastasis potential is a critical point for malignant tumors. Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) is a potential tumor suppress gene and frequently down-regulated in malignant tumors. It has been implicated that overexpression of MDA-7 led to proliferation inhibition in many types of human tumor. Invasion is an important process which is potential to promote tumor metastasis. However, the role and potential molecular mechanism of mda-7/IL-24 to inhibit the invasion of human melanoma cancer is not fully clear. In this report, we identified a solid role for mda-7/IL-24 in invasion inhibition of human melanoma cancer LiBr cells, including decreasing of adhesion and invasion in vitro, blocking cell cycle, down-regulating the expression of ICAM-1, MMP-2/9, CDK1, the phosphorylation of ERK and Akt, NF-kappaB and AP-1 transcription activity. Meanwhile, there was an increased expression of PTEN in mda-7/IL-24 over-expression LiBr cells. Our results demonstrated that mda-7/IL-24 is a potential invasion suppress gene, which inhibits the invasion of LiBr cells by the down-regulation of ICAM-1, MMP-2/9, PTEN, and CDK1 expression. The molecular pathways involved were the MAPK/ERK, PI3K-Akt, NF-kappaB, and AP-1. These findings suggest that mda-7/IL-24 may be used as a possible therapeutic strategy for human melanoma cancer.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Fosforilação
/
Regulação para Baixo
/
Regulação para Cima
/
Movimento Celular
/
NF-kappa B
/
Proteína Quinase CDC2
/
Interleucinas
/
Fator de Transcrição AP-1
/
Molécula 1 de Adesão Intercelular
/
Metaloproteinase 2 da Matriz
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Journal of Korean Medical Science
Ano de publicação:
2013
Tipo de documento:
Article