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Sodium nitrite induces epithelial-mesenchymal transition of SMMC-7721 cells / 药学学报
Acta Pharmaceutica Sinica ; (12): 507-512, 2011.
Artículo en Chino | WPRIM | ID: wpr-348927
ABSTRACT
This study is to find out the induction by sodium nitrite of epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma cells, SMMC-7721. After treatment of SMMC-7721 with 0.25 - 25 mmol.L-1 sodium nitrite for 48 h, the assays used include enzyme-linked immunosorbent assay (ELISA) for evaluation of TGF-beta1, IL-6 and IL-8 level in the conditioned medium, phase-contrast microscopy for morphology observation, and scratch wound healing as well as transwell migration assays for measurement of migration and metastatic potential. Additionally, the hallmarks of EMT, p-AKT and its downstream signaling molecules were examined by Western blotting. The results showed that TGF-beta1 secreted by SMMC-7721 elevated significantly in a dose-dependent fashion, whereas the increased IL-8 and IL-6 did not show dose-dependent response. The EMT was induced by exposure of SMMC-7721 with 0.25 mmol.L-1 of sodium nitrite, which was characterized by increased level of Vimentin, decreased E-cadherin and elevated activity of migration and metastatic potential. The results suggest that sodium nitrite could induce SMMC-7721 EMT by increased secretion of TGF-beta1 and IL-8.
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Farmacología / Nitrito de Sodio / Vimentina / Cadherinas / Movimiento Celular / Interleucina-8 / FN-kappa B / Interleucina-6 / Carcinoma Hepatocelular Límite: Humanos Idioma: Chino Revista: Acta Pharmaceutica Sinica Año: 2011 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Patología / Farmacología / Nitrito de Sodio / Vimentina / Cadherinas / Movimiento Celular / Interleucina-8 / FN-kappa B / Interleucina-6 / Carcinoma Hepatocelular Límite: Humanos Idioma: Chino Revista: Acta Pharmaceutica Sinica Año: 2011 Tipo del documento: Artículo