Killing effect improved by fusion gene HRE1.Egr-1. yCDglyTK on gene-radio therapy of nasopharyngeal cancer in vitro / 中南大学学报(医学版)
Journal of Central South University(Medical Sciences)
; (12): 110-114, 2008.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-814112
Biblioteca responsável:
WPRO
ABSTRACT
OBJECTIVE@#To construct hypoxia/radiation inducible promotor HRE1.Egr-1, and to observe its promotive effect on the expression of yCDglyTK gene in nasopharyngeal cancer HNE-1 cells and the anti-tumor effect of yCDglyTK and to lay an experimental foundation for further exploration of new gene-radio therapy of nasopharyngeal cancer.@*METHODS@#pcDNA3.1(-)HRE1.Egr-1.yCDglyTK was constructed by gene recombination technique. Stable yCDglyTK-expressing HNE-1 cells were generated by transfecting the recombinant plasmid into the target cells with liposome. The expression of yCDglyTK was detected by Western blot in 4 groups a normoxia group, a radiation group, a hypoxia group, and a hypoxia and radiation group. The killing effect of 5-FC in different circumstances was determined by MTT.@*RESULTS@#The expression of yCDglyTK/5-FC gene in all the groups was significantly different(P<0.01),especially in the hypoxia and radiation group. The killing effect of 5-FC on HNE1 cells varied under different conditions, especially in the hypoxia and radiation group.@*CONCLUSION@#Hypoxia and radiation can induce the activity of fusion promoter HRE1.Egr-1, and obviously promote the anti-tumor effect of yCDglyTK/5-FC system, suggesting that yCDglyTK may be a candidate suicide gene for gene-radio therapy of NPC.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Fisiologia
/
Radioterapia
/
Terapêutica
/
Timidina Quinase
/
Células Tumorais Cultivadas
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Terapia Genética
/
Neoplasias Nasofaríngeas
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Elementos de Resposta
/
Subunidade alfa do Fator 1 Induzível por Hipóxia
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Central South University(Medical Sciences)
Ano de publicação:
2008
Tipo de documento:
Artigo