机构地区:[1]上海第二医科大学附属仁济医院消化内科上海市消化疾病研究所,200001
出 处:《中华消化杂志》2004年第3期154-157,共4页Chinese Journal of Digestion
基 金:德国大众基金会资助 ( grantI/75 890 );国家教委青年骨干教师项目资助
摘 要:目的 探讨不同胃癌细胞株对细小病毒细胞毒作用的敏感性差异及可能的机制。方法 共选用HGC2 7(未分化 )、BGC82 3(未分化 )、MKN4 5 (低分化 )、AGS(低分化 )、SGC790 1(中分化 )和MKN2 8(高分化 )等 6株不同分化状态的胃癌细胞株 ,用流式细胞仪分析其各自的细胞周期 ,H 1病毒感染后采用MTT方法检测不同胃癌细胞株对其细胞毒作用的敏感性差异 ,用RT PCR来检测H 1病毒中的非结构蛋白基因 (NS 1)在 6株不同胃癌细胞中的表达。结果 HGC2 7、BGC82 3、MKN4 5、AGS、SGC790 1和MKN2 8等不同分化状态细胞株中 ,S期细胞的比率分别为 2 4 .72 % ,30 .15 % ,2 7.10 % ,2 9 .0 3% ,31.82 %和 33.73%。其中HGC2 7细胞对H 1病毒的细胞毒作用敏感 ;SGC790 1细胞其次 ;MKN4 5、AGS细胞对H 1病毒的细胞毒作用中等敏感 ;MKN2 8细胞对H 1病毒的细胞毒作用不敏感 ;而BGC82 3则对H 1病毒的细胞毒作用抵抗。病毒NS 1的mRNA在HGC2 7、BGC82 3、MKN4 5和SGC790 1等细胞中的表达水平较高 ,而在AGS和MKN2 8中的表达水平却较低。结论 H 1病毒的细胞毒作用在不同的胃癌细胞株中的差异显著。总体上 ,与高分化细胞株MKN2 8细胞相比 ,分化差的细胞对细小病毒H 1的细胞毒作用敏感性增加。其机制至少部分与分化差细胞中病毒NSObjective To investigate the sensitivities of distinct gastric cancer cells to parvovirus H-1 induced cytotoxicity and its possible mechanisms. Methods Six distinct differentiated gastric cancer cell lines were employed in this study, including HGC27 (undifferentiated), BGC823(undifferentiated), MKN45(poor differentiated), AGS (poor differentiated), SGC7901(moderate differentiated) and MKN28 (well differentiated). The cell cycle distributions were measured by flow cytometry. The differential sensitivities of six distinct gastric cancer cells after H-1 virus infection were detected by MTT analysis. The RT-PCR was employed to detect viral NS-1 gene expression in all six gastric cancer cell lines. Results The S phase ratios of HGC27, BGC823, MKN45, AGS, SGC7901 and MKN28 were 24.72%, 30.15%, 27.10%, 29.03%, 31.82% and 33.73% respectively. HGC27 cells were sensitive to H-1 virus induced cytotoxicity followed by SGC7901 cells. MKN45 and AGS cells were moderately sensitive. MKN28 cells were insensitive. However, BGC823 cells were resistant to H-1 virus induced cytotoxicity. The expressions of viral NS-1 were higher in HGC27, BGC823, MKN45 and SGC7901 cells, whilst NS-1 gene expressions were lower in AGS and MKN28 cells. Conclusions The sensitivities of distinct gastric cancer cells to H-1 virus induced cytotoxicity could be markedly different. In general, the poorly differentiated cells showed an enhanced sensitivity to H-1 virus attack as compared to well differentiated ones. The enhanced sensitivity of poorly-versus well-differentiated gastric cancer cells to H-1 virus is due to at least in part, to the enhanced capacity of the former cells for NS-1 protein production and accumulation. The undifferentiated BGC823 cells were resistant to H-1 virus triggered cytotoxicity. It may further verify that not all the tumor cells were sensitive to H-1 virus lytic effects.
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