Down regulation of mitogen activated protein kinase phosphatase-1 mediate acquired multidrug resistance in pancreatic adenocarcinoma cell line SW1990/Fu / 中华外科杂志
Chinese Journal of Surgery
;
(12): 473-475, 2006.
Artigo
em Chinês
| WPRIM
| ID: wpr-317130
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of mitogen activated protein kinase phosphatase-1 (MKP-1) in mediating acquired multidrug resistance in pancreatic adenocarcinoma cell line SW1990/Fu.</p><p><b>METHODS</b>To detect MKP-1 mRNA expression, Northern blot analysis was carried out in well established drug resistant pancreatic adenocarcinoma cell line SW1990/Fu, SW1990 and MiaPaCa-2 cell lines. To further elucidate the exact role of MKP-1, Western blot hybridization was performed in these three cell lines.</p><p><b>RESULTS</b>Northern blot analysis of total RNA isolated from SW1990/Fu, SW1990 and MiaPaCa-2 cell lines revealed the presence of the 2400 bp MKP-1 transcript 7 at relatively high levels in pancreatic cancer cell lines SW1990 and MiaPaCa-2. In the SW1990/Fu, the MKP-1 transcript was detectable at very low level. Densitometric analysis with normalization to 7S indicated that MKP-1 mRNA expression level was significantly decreased in SW1990/Fu in comparison with the parental and MiaPaCa-2 cell lines. MKP-1 protein expression level in SW1990/Fu detected by Western blot was coincident with mRNA level.</p><p><b>CONCLUSIONS</b>MKP-1 may be involved in acquired multidrug resistance in pancreatic adenocarcinoma, and we could hypothesized that alterations of intra-cellular transduction signal system acts as an important role in multidrug resistance of tumor cells.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Neoplasias Pancreáticas
/
Patologia
/
Fisiologia
/
RNA Mensageiro
/
Adenocarcinoma
/
Regulação para Baixo
/
Western Blotting
/
Northern Blotting
/
Proteínas Tirosina Fosfatases
/
Proteínas Imediatamente Precoces
Limite:
Humanos
Idioma:
Chinês
Revista:
Chinese Journal of Surgery
Ano de publicação:
2006
Tipo de documento:
Artigo
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