首页|RNAi抑制皮肤鳞癌A431细胞EGFR表达的实验研究

RNAi抑制皮肤鳞癌A431细胞EGFR表达的实验研究

扫码查看
目的:研究RNA干扰(RNA interference,RNAi)对皮肤鳞癌A431细胞表皮生长因子受体(EGFR)基因表达的抑制作用及其对A431细胞增殖、凋亡的影响.方法:设计制备两对针对EGFR基因的小干扰RNA(small interfering RNA,siRNA),转染A431人皮肤鳞癌细胞株,采用RT-PCR法检测EGFR mRNA的表达;Western Blot测定EGFR蛋白的表达;MTT法检测细胞生长的影响;流式细胞仪检测细胞凋亡率.结果:siRNA2干扰后EGFR mRNA与蛋白的表达强度分别为(16.5±1.6)%和(11.1±1.6)%,与对照组比较有统计学差异(P<0.05);在EGFR表达受到抑制的同时,转染后的A431胞生长速度明显变慢;A431细胞的凋亡率为(12.6±1.4)%,与对照组比较有统计学差异(P<0.05).结论:siRNA2能有效抑制皮肤鳞癌细胞EGFR基因的表达,抑制细胞的增殖,并促进细胞凋亡.
Inhibitory effects of siRNA on expression of epidermal growth factor receptor in squamous cell carcinoma cell line A431
AIM: To investigate the inhibitory effect of RNA interference ( RNAi) on the epidermal growth factor receptor (EGFR) gene expression in A431 cell line. METHODS: Two pairs of small interfering RNA ( siRNA) for EGFR gene were designed and transfected into A431 cells. EGFR gene expression was assessed by RT-PCR and EGFR protein expression was tested by Western blot. The proliferation of the A431 cells was detected by MTT method and flow cytometry was used to measure the cell apoptosis. RESULTS: The expression rates of EGFR mRNA and the expression rates of EGFR protein were (16. 5 ± 1. 6 ) % and (11.1 ±1.6)%,respectively in A431 EGFR siRNA2-transfected cells,significantly lower than those of control cells (P < 0. 05). Obvious decrease in growth of the A431 cells was observed after transfected with EGFR siRNA2 and the apoptosis rate was (12.6 ±1.4)%,significantly higher than that of control cells (P < 0.05). CONCLUSION: siRNA effectively inhibits the transcription and the expression of EGFR gene in the squamous cell carcinoma cell line A431. siRNA increases apoptosis index of the A431 cells and inhibits their growth.

RNA interferenceepidermal growth factor receptorsquamous cell carcinomaapoptosis

吴波、郑锦芬、余振东、江智茂、马刚

展开 >

北京大学深圳医院皮肤科,广东,深圳,518036

北京大学深圳医院检验科,广东,深圳,518036

北京大学深圳医院中心实验室,广东,深圳,518036

RNA干扰 表皮生长因子受体 鳞状细胞癌 细胞凋亡

深圳市科技计划项目

200802019

2009

第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
年,卷(期):2009.30(12)
  • 1
  • 1