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作 者:李丽媛 聂子元[1] 张小艳[1] 罗建民[1] 杨琳[1] 王茜[1] LI Li-Yuan;NIE Zi-Yuan;ZHANG Xiao-Yan;LUO Jian-Min;YANG Lin;WANG Qian(Department of Hematopathology,The Second Hospital of Hebei Medical University,Hematology Key Laboratory of Hebei Province,Shijiazhuang 050000,Hebei Province,China)
机构地区:[1]河北医科大学第二医院血液内科,河北省血液病重点实验室,河北石家庄050000
出 处:《中国实验血液学杂志》2023年第4期1038-1043,共6页Journal of Experimental Hematology
基 金:河北省医学科学研究课题(20190051)。
摘 要:目的:建立抑制同源盒基因1(SIX1)表达的HL-60细胞及耐阿霉素的HL-60细胞(HL-60/ADR),研究抑制SIX1对HL-60及HL-60/ADR细胞耐药作用的影响。方法:用慢病毒感染HL-60及HL-60/ADR细胞,经嘌呤霉素筛选获得稳定抑制SIX1表达的细胞株。采用CCK-8法检测各组细胞的增殖能力,流式细胞凋亡试剂盒检测细胞凋亡情况,实时定量PCR检测耐药相关基因的表达水平。结果:成功构建了抑制SIX1表达的HL-60及HL-60/ADR稳定转染细胞株。与对照组相比较,抑制SIX1的表达使HL-60及HL-60/ADR细胞的增殖明显受抑制(P<0.05),细胞的凋亡率显著增加(P<0.05),并且抑制SIX1表达后细胞对阿霉素的敏感性升高。结论:抑制SIX1的表达可以提高细胞对阿霉素的敏感性,其逆转耐药性的作用可能与促进细胞凋亡基因的表达有关。Objective:To establish HL-60 cells and adriamycin resistant HL-60 cells(H-60/ADR)in which the expression of homologous box gene 1(SIX1)was inhibited,and investigate the effect of inhibiting the expression of SIX1 on the drug resistance.Methods:Lentivirus was used to transfect HL-60 and HL-60/ADR cells,and the cell lines stably inhibiting the expression of SIX1 were screened by puromycin.CCK-8 assay was used to detect the proliferation ability of cells in each group,apoptosis kit was used to detect the cell apoptosis,and real-time quantitative PCR was used to detect the expression level of drug-resistant related genes.Results:HL-60 and HL-60/ADR stably transfected cell lines with down-regulation of SIX1 expression were successfully constructed.Compared with control group,the inhibition of SIX1 expression significantly inhibited the proliferation of HL-60 and HL-60/ADR cells(P<0.05),increased the apoptosis rate(P<0.05),and the sensitivity of cells to adriamycin increased after inhibition of SIX1 expression.Conclusion:Inhibition of SIX1 expression can improve cell sensitivity to adriamycin,and its role in reversing drug resistance may be related to the promotion of apoptosis gene expression.
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