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Effect of Inhibiting SIX1 Expression on Drug-resistance of Acute Myeloid Leukemia Cell Line HL-60/ADR Cells / 中国实验血液学杂志
Journal of Experimental Hematology ; (6): 1038-1043, 2023.
Article in Chinese | WPRIM | ID: wpr-1009961
ABSTRACT
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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Full text: Available Index: WPRIM (Western Pacific) Main subject: Leukemia, Myeloid, Acute / Doxorubicin / Apoptosis / Homeodomain Proteins / HL-60 Cells / Drug Resistance, Neoplasm / Cell Proliferation Limits: Humans Language: Chinese Journal: Journal of Experimental Hematology Year: 2023 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Leukemia, Myeloid, Acute / Doxorubicin / Apoptosis / Homeodomain Proteins / HL-60 Cells / Drug Resistance, Neoplasm / Cell Proliferation Limits: Humans Language: Chinese Journal: Journal of Experimental Hematology Year: 2023 Type: Article