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作 者:刘丽[1] 沈洪[1] 姜鹏君[1] 陈劼[1] 刘青[2] 张旭[3]
机构地区:[1]南京中医药大学附属医院,江苏南京210029 [2]江苏第二师范学院江苏省生物功能分子重点建设实验室,江苏南京210013 [3]南京中医药大学江苏省中医药防治肿瘤协同创新中心,江苏南京210023
出 处:《南京中医药大学学报》2016年第3期264-268,共5页Journal of Nanjing University of Traditional Chinese Medicine
基 金:欧盟第七框架项目(PIRSES-GA-2013-612589);江苏省高校优势学科建设工程资助项目(PAPD);科技部"十一五"支撑计划(2006BAI11B08-01)
摘 要:目的研究异甘草素对人非小细胞肺癌NCI-H157细胞增殖、凋亡及细胞内质网应激相关基因ATF4、DDIT3和TNFRSF10B表达的影响。方法体外培养NCI-H157细胞,给予异甘草素处理,MTT法检测不同浓度的异甘草素对NCI-H157细胞的增殖抑制率,流式细胞术检测不同浓度异甘草素对肿瘤细胞的凋亡发生率,实时定量PCR检测NCI-H157细胞在不同浓度异甘草素处理后ATF4、DDIT3和TNFRSF10B基因mRNA的表达。结果在一定浓度范围内,异甘草素能显著抑制人肺癌NCI-H157细胞的增殖,并呈时间与剂量依赖性。异甘草素能显著诱导NCI-H157细胞凋亡的发生,并上调ATF4、DDIT3和TNFRSF10B基因在细胞内的表达(P〈0.05-0.01)。结论异甘草素能够抑制人肺癌NCI-H157细胞的增殖,诱导凋亡发生,且与激活内质网应激反应有关。OBJECTIVE To study the effect of isoliquiritigenin on cell proliferation,apoptosis induction,mRNA expression of endoplasmic reticulum stress related gene ATF4,DDIT3 and TNFRSF10Bin NCI-H157 human lung cancer cell line.METHODS NCI-H157 cells were cultured and treated with various concentrations isoliquiritigenin.The cell proliferation was analyzed by MTT and the occurrence of cell apoptosis was examined by flow cytometry.ATF4,DDIT3 and TNFRSF10Bgene mRNA expression were detected by real-time fluorescence quantitative polymerase chain reaction.RESULTS Isoliquiritigenin significantly inhibited NCI-H157 cell proliferation in a dose and time dependent manner.The results of flow cytometry revealed that isoliquiritigenin could induce apoptosis in NCI-H157 cells.Real-time quantitative RT-PCR showed that isoliquiritigenin up?regulated mRNA expression of ATF4,DDIT3 and TNFRSF10B(P〈0.05-0.01).CONCLUSION Isoliquiritigenin can inhibit NCI-H157 cell proliferation,induce cell apoptosis by activating the endoplasmic reticulum stress response.
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