Visfatin Triggers the Cell Motility of Non-Small Cell Lung Cancer via Up-Regulation of Matrix Metalloproteinases.
Basic Clin Pharmacol Toxicol
; 119(6): 548-554, 2016 Dec.
Article
em En
| MEDLINE
| ID: mdl-27224551
ABSTRACT
High levels of visfatin are correlated with worse clinical prognosis of various cancers. Still, the effects and mechanisms of visfatin on progression of non-small cell lung cancer (NSCLC) remain unclear. This study revealed that plasma levels of visfatin in patients with NSCLC (585 ± 287 pg/ml) were significantly (p < 0.01) higher than those in healthy people (142 ± 61.1 pg/ml). The high level of plasma visfatin was found to be significantly (p < 0.05) correlated with TNM stage, lymph node metastasis and distant metastasis. Visfatin treatment can increase the migration and invasion of NSCLC cells via up-regulation of metalloproteinase-2 (MMP-2) and MMP-9. Both si-MMP-2 and si-MMP-9 attenuated visfatin-induced migration of NSCLC cells. The inhibitor of NF-κB, while not ERK1/2, p38-MAPK or PI3K/Akt, can significantly abolish visfatin-induced migration of A549 cells and up-regulation of MMP-2 and MMP-9. Furthermore, visfatin can increase the phosphorylation of IκBα and p65 and the transcription activities of NF-κB in NSCLC cells. ACHP, the inhibitor of IKK-ß, blocked visfatin-induced activation of p65 and up-regulation of MMP-2 and MMP-9. Collectively, our data revealed that visfatin can trigger the in vitro migration and invasion of NSCLC cells via up-regulation of MMPs through activation of NF-κB.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Regulação para Cima
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Indução Enzimática
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Citocinas
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Carcinoma Pulmonar de Células não Pequenas
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Metaloproteinase 2 da Matriz
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Metaloproteinase 9 da Matriz
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Nicotinamida Fosforribosiltransferase
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Neoplasias Pulmonares
Tipo de estudo:
Prognostic_studies
Limite:
Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Basic Clin Pharmacol Toxicol
Ano de publicação:
2016
Tipo de documento:
Article