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.
题目: 抑制SIX1表达对急性髓系白血病耐药细胞HL-60/ADR的影响.
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。.
Keywords: acute myeloid leukemia; drug resistance; drug-resistant cell; homologous box gene 1.