Effect and mechanisms of TET on human gastric carcinoma cell line SGC7901 and SGC7901/ADR / 中国中西医结合杂志
Zhongguo Zhong Xi Yi Jie He Za Zhi
; (12): 66-70, 2014.
Article
em Zh
| WPRIM
| ID: wpr-231599
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of tetrandrine (TET) on zinc finger protein 139 (ZNF139) and multidrug resistance (MDR) of human gastric carcinoma cell lines and possible mechanisms.</p><p><b>METHODS</b>Cultured SGC7901 and SGC7901/ADR were treated with TET (0.5, 1.0, 1.5, 2.0, and 2.5 microg/mL), then inhibition rates were measured by MTT assay in vitro. The expressions of ZNF139, MRP-1, MDR1, and GST-pi were detected by RT-PCR. The correlation between ZNF139 and each multidrug resistance factor was analyzed using Spearman correlation analysis, and the coefficient correlation was calculated.</p><p><b>RESULTS</b>The inhibition rate of TET (< or = 2.0 microg/mL) for SGC7901 and SGC7901/ADR was less than 10% with MTT assay. Expressions of ZNF139, MRP-1, MDR1, and GST-pi mRNA were higher in SGC7901/ADR than in SGC7901 (all P < 0.05). The expressions of ZNF139, MRP-1, MDR1, and GST--pi were down-regulated in SGC7901/ADR cells efficiently (all P < 0.01). Positive correlation existed between ZNF139 and MRP-1, ZNF139 and MDR1 before treated by TET in SGC7901/ADR, and this relationship also existed in SGC7901/ADR cells after treated by TET (all P < 0.05).</p><p><b>CONCLUSION</b>TET could achieve MDR reversion in gastric cancer cells by down-regulating the expression of ZNF139, MRP-1, and MDR1.</p>
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Farmacologia
/
Neoplasias Gástricas
/
Dedos de Zinco
/
Resistência a Múltiplos Medicamentos
/
Resistencia a Medicamentos Antineoplásicos
/
Subfamília B de Transportador de Cassetes de Ligação de ATP
/
Proteínas Associadas à Resistência a Múltiplos Medicamentos
/
Linhagem Celular Tumoral
/
Benzilisoquinolinas
/
Fatores de Transcrição Kruppel-Like
Limite:
Humans
Idioma:
Zh
Revista:
Zhongguo Zhong Xi Yi Jie He Za Zhi
Ano de publicação:
2014
Tipo de documento:
Article