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干扰素-α通过上调DR5和抑制Akt的活性增加胃癌细胞对TRAIL的敏感性 被引量：1

Interferon-α sensitized human gastric cancer cells to TRAIL-induced apoptosis via upregulation of DR5 and inhibition the activity of Akt
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摘要 目的:观察IFN-α对TRAIL诱导胃癌细胞凋亡的影响,并对死亡受体DR5和PI3K/Akt通路在此过程中的作用机制进行探讨。方法:MTT法检测细胞增殖能力,流式细胞仪PI染色检测细胞凋亡,蛋白质印迹法检测蛋白的表达。结果:IFN-α预处理可协同TRAIL抑制胃癌MGC803细胞增殖。单独用IFN-α或TRAIL处理MGC803细胞,仅有少量的细胞发生凋亡,IFN-α和TRAIL联合用药细胞凋亡明显增加(P<0.01)。IFN-α能上调DR5的表达,抑制Akt的磷酸化。结论:IFN-α能增强TRAIL诱导的胃癌细胞凋亡,其机制可能与其上调DR5的表达和抑制Akt的活性有关。 Objective：To investigate the effect of IFN-α on TRAIL-induced apoptosis of gastric cancer and evaluate the role of death receptor DR5 and PI3K/Akt pathway during the process.Methods： Cell proliferation was measured by MTT assay and cell apoptosis was determined by flow cytometry using propidium iodide staining.Protein expression was assayed by Western blot.Results： In gastric cancer MGC803 cells,preincubation with IFN-α enhanced the TRAIL-induced cytotoxicity.Only slight cell apoptosis was induced by IFN-α alone and TRAIL alone.In contrast,pretreatment of cells with IFN-α significantly amplified TRAIL-induced cell apoptosis.IFN-α upregulated DR5 expression and inhibited the activity of Ak.Conclusion： IFN-α enhanced TRAIL-induced apoptosis in gastric cancer cells might be correlated with upregulation of DR5 and inhibition of PI3K/Akt pathway.
作者 曲晶磊 唐冰 刘云鹏 曲秀娟 侯科佐
机构地区 中国医科大学附属第一医院肿瘤内科 中国医科大学附属第一医院麻醉科
出处 《现代肿瘤医学》 CAS 2012年第4期655-658,共4页 Journal of Modern Oncology
基金 国家自然科学基金资助项目(编号:31000607)
关键词 肿瘤坏死因子相关凋亡诱导配体 干扰素Α 死亡受体5 PI3K/AKT通路 胃癌 TRAIL IFN-α DR5 PI3K/Akt gastric cancer
分类号 R73-362 [医药卫生—肿瘤] R735.2 [医药卫生—肿瘤]
  • 相关文献

参考文献11

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二级参考文献13

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共引文献2

同被引文献35

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现代肿瘤医学
2012年 第4期

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