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目的 观察Fas基因转导人胃癌耐药细胞SGC790 1/VCR对化疗药物的敏感性 ,并初步探讨其机制。方法 以流式细胞仪检测Fas基因转导和对照胃癌细胞在细胞周期中的分布 ;用MTT实验检查癌细胞对多种药物的敏感性 ;用免疫细胞化学染色法检测胃癌细胞P 糖蛋白 (P gp)和拓扑异构酶II(TopoII)的表达。结果 与胃癌细胞SGC790 1和pBK SGC790 1/VCR相比较 ,Fas SGC790 1/VCR在G2期减少 ,S期增多 ,并出现明显的凋亡峰 ;Fas SGC790 1/VCR对DDP ,MMC和 5 Fu的敏感性增加 ,但对VCR和DOX的敏感性无明显变化 ;SGC790 1,pBK SGC790 1/VCR和Fas SGC790 1/VCRTopoII的表达无明显差别 ;Fas SGC790 1/VCRP gp的表达水平明显低于 pBK SGC790 1/VCR ,仅显示弱阳性。 结论 Fas基因可在一定程度上逆转人胃癌耐药细胞SGC790 1/VCR的多药耐药性 (MDR) ,其涉及的相关机制可能是增强细胞对凋亡诱导剂的敏感性 ,以及降低细胞P gp的表达水平
Objective To observe the sensitivity of Fas-transduced human gastric cancer-resistant cell line SGC790 1/VCR to chemotherapeutics and to explore its mechanism. Methods Flow cytometry was used to detect the distribution of Fas gene transduction and control gastric cancer cells in the cell cycle; MTT assay was used to examine the sensitivity of cancer cells to multiple drugs; and immunocytochemical staining was used to detect gastric cancer cell P glycoprotein (P). Expression of gp) and topoisomerase II (Topo II). Results Compared with gastric cancer cells SGC790 1 and pBK SGC790 1/VCR, Fas SGC790 1/VCR decreased in G2 phase, increased in S phase, and showed significant apoptotic peaks; Fas SGC790 1/VCR on DDP, MMC and 5 Fu Sensitivity increased, but there was no significant change in sensitivity to VCR and DOX; SGC790 1, pBK SGC790 1/VCR and Fas SGC790 1/VCR TopoII expression was not significantly different; Fas SGC790 1/VCRP gp expression was significantly lower than pBK SGC790 1/VCR, only weakly positive. Conclusion The Fas gene can reverse the multidrug resistance (MDR) of human gastric cancer-resistant SGC790 1/VCR to a certain extent. The mechanism involved may be to increase the sensitivity of cells to apoptosis-inducing agents and to decrease the number of cells. Gp expression level