摘要
目的探讨RNA干扰核苷酸剪切修复偶联因子1(ERCC1)基因表达对人卵巢癌耐药细胞DDP、PGPIPN敏感性的影响。方法实验分为空白对照组、特异性转染组和非特异性转染组。采用MTT法测定PGPIPN、DDP对3组细胞的增殖抑制率,RT-PCR法检测PGPIPN对3组细胞乳腺癌易感基因1(BRCA1)基因表达的影响。结果 MTT法结果显示,PGPIPN作用人卵巢癌耐药细胞SKOV3/DDP 48 h,对其增殖有一定的抑制作用,在浓度为40、60 mg/L时,与浓度为0 mg/L比较,差异有统计学意义(P<0.05);DDP、PGPIPN分别作用特异性转染组细胞48 h,其增殖明显受到抑制,与0 mg/L比较,差异均有统计学意义(P<0.05);RTPCR法结果显示,PGPIPN作用特异性转染组细胞48 h,其BRCA1基因表达随着PGPIPN浓度升高而明显降低,在浓度为40、60 mg/L时,与PGPIPN浓度为0 mg/L比较,差异有统计学意义(P<0.01)。结论 PGPIPN对SKOV3/DDP细胞的增殖有一定的抑制作用,并且通过干扰ERCC1基因表达可以明显增强SKOV3/DDP细胞对DDP、PGPIPN的敏感性,同时可增强PGPIPN对BRCA1基因的下调水平。
Objective To investigate the effects of gene expression of RNA interfering nucleotide excision repair cross-complementation 1（ ERCCl）on DDP,PGPIPN sensitivity in human ovarian cancer drug resistance cell. Methods In the test,there were blank control group,specificity transfection group and non-specificity transfection group. MTT method was used to determine the effects of PGPIPN,DDP on cell proliferation inhibition rate for the three groups;RT-PCR method was used to test the effects of PGPIPN on gene expression of breast cancer suscepti-bility gene 1（BRCAl）in cell of the three groups. Results MTT results showed that PGPIPN affected human ovari-an cancer drug resistance cell for 48 h,and provided certain inhibition for their proliferation,which was statistically significant at 40,60 mg / L of concentration compared to 0 mg / L（P 〈 0. 05）;DDP and PGPIPN affected cell for 48 h respectively in the specificity transfection group,in which the cell proliferation was significantly inhibited,both of which had statistically significant differences compared to 0 mg / L of DDP,PGPIPN concentration（P 〈 0. 05）;RT-PCR results showed that PGPIPN affected cells for 48 h in specificity transfection group,BRCAl gene expression of which significantly decreased with the increase of PGPIPN concentration,having statistically significant differences at 40,60 mg / L of concentration compared to 0 mg / L of PGPIPN concentration（P 〈 0. 01）. Conclusion PGPIPN has certain inhabitation effect on the proliferation of SKOV3 / DDP,and it can significantly enhance the DDP and PGPIPN sensitivity by interference ERCCl gene expression of SKOV3 / DDP. Meanwhile,it can enhance PGPIPN down-regulate the level of BRCAl gene expression.
出处
《安徽医科大学学报》
CAS
北大核心
2015年第6期730-734,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金(编号:81472448)
