Effect of oxaliplatin on the survival rate of human Y79 cells after down-regulation of Mcl-1 / 国际眼科杂志(Guoji Yanke Zazhi)
International Eye Science
;
(12): 2226-2228, 2017.
Artigo
em Chinês
| WPRIM
| ID: wpr-669410
ABSTRACT
·AIM:
To study the effect of oxaliplatin on the survival rate of Y79 after down-regulation of Mcl-1 by SiRNA.·METHODS:
Y79 cells were cultured in RPMI1640. The cultured cells were stimulated with 0. 25μmol/L of oxaliplatin. The expression of Mcl - 1 protein was detected by Western blot after 6, 16 and 24h respectively. Cells in logarithmic phase were collected and used for single-cell suspension. Then they were transfected with empty plasmid, Mcl-1-homo-991, Mcl-1-homo-1114 and Mcl - 1 - homo - 1235. After 6h, fluorescence microscope was used to observe the transfection efficiency and the optimal one was selected. The cells were divided into Group A and transfected with empty plasmids. The cells transfected with Mcl-1 were divided into Group B and Group C. Group A and Group C were treated with 0. 25μmol/L oxaliplatin for stimulating induction, and the apoptotic rate was compared after 24h.·RESULTS:
The expression of Mcl-1 in Y79 stimulated by oxaliplatin was the most after 24h of culture. Mcl-1-homo-991 significantly inhibited the expression of Mcl-1 in Y79 after transfection. There was no significant difference in the apoptosis rate in Group A ( 11. 1% ± 1. 2%) and in the control group (6. 1%±0. 6%)(P>0. 05). The apoptotic rate of Group C ( 49. 2% ± 2. 7%) was significantly higher than that of Group B (20. 8%±1. 9%).At the same time, the apoptotic rates of these two groups were significantly higher than those of Group A and control group, the difference was statistically significant (P<0. 05).·CONCLUSION:
Downregulation of Mcl-1 by siRNA can reduce the drug resistance of Y79, thereby enhancing the apoptosis of Y79, and reducing the survival rate of Y79.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
International Eye Science
Ano de publicação:
2017
Tipo de documento:
Artigo
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