苯醌类安沙霉素药物17AAG调节胃癌细胞株恶性生物学行为的实验研究

Regulation of benzoquinones ansamycins 17AAG on malignant biological behaviors of gastric cancer cell lines

目的:研究苯醌类安沙霉素药物17AAG对胃癌细胞株恶性生物学行为的调节作用。方法:培养胃癌细胞株SGC7901,用0、5、10、20、40μmol/L的17AAG处理后,测定细胞周期、凋亡细胞比例以及肿瘤坏死因子相关凋亡诱导配体(TRAIL)、Fas、FasL、多发性内分泌肿瘤1型(MEN1)、WTX、硫氧还蛋白结合蛋白(TXNIP)、髓样细胞白血病蛋白-1(MCL-1)、DEK、生存素(Survivin)、锌指蛋白139(ZNF139)、CyclinD1、增殖细胞核抗原(PCNA)的含量。结果:不同剂量17AAG组间G1期细胞的比例无显著差异,G2/M期细胞的比例、S期细胞的比例以及早期凋亡率、晚期凋亡率、总凋亡率有显著性差异(P<0.05),17AAG剂量越大,G2/M期细胞的比例越低,S期细胞的比例以及早期凋亡率、晚期凋亡率、总凋亡率越高;40μmol/L 17AAG组细胞中TRAIL、Fas、FasL、MEN1、WTX、TXNIP的含量显著高于0μmol/L 17AAG组(P<0.05),MCL-1、DEK、Survivin、ZNF139、CyclinD1、PCNA的含量显著低于0μmol/L17AAG组(P<0.05)。结论:苯醌类安沙霉素药物17AAG能够抑制胃癌细胞株的恶性生物学行为,抑制细胞周期、诱导细胞凋亡。

Objective：To study the regulating effect of benzoquinones ansamycins 17 AAG on malignant biological behaviors of gastric cancer cell lines.Methods：Gastric cancer cell lines SGC7901 were cultured and treated with 0μmol/L,5μmol/L,10μmol/L,20μmol/L and 40μmol/L 17 AAG,and then percentage of cell cycle and apoptotic cell as well as contents of TRAIL,Fas,FasL,MEN1,WTX,TXNIP,MCL-1,DEK,Survivin,ZNF139,CyclinD1 and PCNA were detected.Results：Percentage of cells in G1 phase was without significant differences among different doses of 17 AAG groups,the percentage of cells in G2/M phase and the percentage of cells in S phase as well as early apoptotic rate,late apoptotic rate and total apoptotic rate were significantly different,and the larger the 17 AAG dose,the lower the percentage of cells in G2/M phase,the higher the percentage of cells in S phase as well as early apoptotic rate,late apoptotic rate and total apoptotic rate;TRAIL,Fas,FasL,MEN1,WTX and TXNIP contents of 40μmol/L17 AAG group were significantly higher than those of 0μmol/L17 AAG group,and MCL-1,DEK,Survivin,ZNF139,CyclinD1 and PCNA contents were significantly lower than those of 0μmol/L17 AAG group.Conclusions：Benzoquinones ansamycins 17 AAG can inhibit the malignant biological behaviors of gastric cancer cell lines,inhibit cell cycle and induce cell apoptosis.