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Silencing of endothelin-1 suppresses growth, migration, and invasion of nasopharyngeal carcinoma cells in vitro / 南方医科大学学报
Journal of Southern Medical University ; (12): 915-920, 2016.
Artigo em Chinês | WPRIM | ID: wpr-286874
ABSTRACT
<p><b>OBJECTIVE</b>To explore the role of endothelin-1 (ET-1) gene in regulating the proliferation, migration and invasion of nasopharyngeal carcinoma cells.</p><p><b>METHODS</b>A lentivirus-mediated shRNA-ET-1 vector was infected into 5-8F cells, and the interference efficiency was examined with Western blotting. MTT assay, cell cycle analysis, plate colony formation assay, Transwell assay, Boyden chamber assay and tumor growth assay were carried out to analyze the changes in cell proliferation, migration and invasion. The expressions of genes related with epithelial-mesenchymal transition (EMT) were examined using Western blotting.</p><p><b>RESULTS</b>shRNA-ET-1 transfection significantly inhibited the expression of ET-1, and suppressed the growth, migration and invasion of 5-8F cells. ET-1 knockdown enhanced the expression of E-cadherin and CK18 and inhibited the expression of N-cadherin and vimentin.</p><p><b>CONCLUSION</b>ET-1 promotes cell growth, migration and invasion by modulating the genes associated with epithelial-mesenchymal transition in nasopharyngeal carcinoma cells.</p>
Assuntos
Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Vimentina / Carcinoma / Transfecção / Antígenos CD / Caderinas / Ciclo Celular / Movimento Celular / Neoplasias Nasofaríngeas / Lentivirus Limite: Humanos Idioma: Chinês Revista: Journal of Southern Medical University Ano de publicação: 2016 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Assunto principal: Patologia / Vimentina / Carcinoma / Transfecção / Antígenos CD / Caderinas / Ciclo Celular / Movimento Celular / Neoplasias Nasofaríngeas / Lentivirus Limite: Humanos Idioma: Chinês Revista: Journal of Southern Medical University Ano de publicação: 2016 Tipo de documento: Artigo