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作 者:张迎春[1] 杨群培[1] 唐源[1] 王威亚[1] 于建渤[1] 刘卫平[1]
出 处:《中华肿瘤杂志》2013年第9期651-654,共4页Chinese Journal of Oncology
基 金:国家自然科学基金(30971113、30901690)
摘 要:目的探讨阿霉素对结外鼻型NK/T细胞淋巴瘤SNK-6细胞株肿瘤坏死因子相关凋亡诱导配体(TRAIL)耐受及其受体表达的影响。方法以不同浓度的阿霉素单独或与TRAIL联合作用于SNK-6细胞,采用四甲基偶氮唑蓝(MTT)法检测细胞的生长情况。采用流式细胞术检测SNK-6细胞的凋亡情况和TRAIL受体的表达情况。结果100和1000ng/ml阿霉素单独处理SNK-6细胞24h时,SNK-6细胞的存活率分别为(80.9±7.2)%和(53.7±2.8)%,与联合TRAIL组的差异有统计学意义[分别为(64.9±1.1)%和(34.0±3.9)%,P〈0.05]。100和1000ng/ml阿霉素单独处理SNK-6细胞48h时,SNK-6细胞的存活率分别为(69.9±6.1)%和(31.1±1.9)%,与联合TRAIL组的差异亦有统计学意义[分别为(37.5±6.4)%和(15.0±1.8)%,P〈0.05]。经100和1000ng/ml阿霉素单独处理48h后,SNK-6细胞的早期凋亡率分别为(14.8±0.6)%和(30.8±1.5)%,与联合TRAIL组的差异有统计学意义[分别为(28.7±0.6)%和(46.6±2.8)%,P〈0.05]。经100ng/ml阿霉素处理24h后,SHK-6细胞表面TRAIL死亡受体和欺骗受体的表达明显增加。结论阿霉素在一定程度上可以克服SNK6细胞对TRAIL的耐受,但需要较大剂量的TRAIL才能起作用,这可能与阿霉素同时诱导了TRAIL死亡受体和欺骗受体表达上调有关。Objective To investigate the effect of doxorubicin on TRAIL resistance and TRAIL receptor expression in lymphoma cell line SNK-6 cells. Methods SNK-6 ceils treated with doxorubicin at different concentrations alone or in combination with tumor necrosis factor related apoptosis inducing ligand (TRAIL). Cell proliferation was evaluated by MTr assay. Apoptosis and the expression of TRAIL receptors were determined by flow cytometry. Results MTr assay srhowed that treatment with 100 and 1000 ng/ml doxorubicin for 24 h, the survival rates of SNK-6 cells were ( 80.9 ± 7.2) % and (53.7 ± 2.8 ) %, significantly higher than that by treatment combined with 500 ng/ml TRAIL (64.9 ± 1.1 ) % and (34.0 ± 3.9) %, respectively (P 〈 0.05 ). Flow cytometry showed that after treatment with 100 and 1000 ng/ml doxorubicin for 48 h, the survival rates of SNK-6 cells were ( 69.9 ± 6.1 ) % and ( 31.1 ±1.9 ) %, while treated in combination with 500 ng/ml TRAIL, the cell survival rates were ( 37.5 ±6.4) % and ( 15.0 ±1.8 ) %, respectively. The early apoptosis rate was ( 14.8 ±0.6 ) % and ( 30.8 ±1.5 ) %, significantly lower than that [ (28.7 ±0.6) % and (46.6 ±2.8 ) % ] after treatment in combination with TRAIL ( P 〈 0.05). The expressions of TRAIL receptors and decoy receptors were increased when SNK-6 cells were treated with 100 ng/ml doxorubicin for 24 hours. Conclusions Doxorubicin can overcome to a certain extent the TRAIL resistance of SNK-6 cells and induce upregnlation of TRAIL death receptors and decoy receptors on the surface of SNK-6 cells. However, a higher dose is needed.
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