Effect of Inhibiting SIX1 Expression on Drug-resistance of Acute Myeloid Leukemia Cell Line HL-60/ADR Cells.
10.19746/j.cnki.issn.1009-2137.2023.04.017
- Author:
Li-Yuan LI
1
;
Zi-Yuan NIE
1
;
Xiao-Yan ZHANG
1
;
Jian-Min LUO
2
;
Lin YANG
1
;
Qian WANG
1
Author Information
1. Department of Hematopathology, The Second Hospital of Hebei Medical University, Hematology Key Laboratory of Hebei Province, Shijiazhuang 050000, Hebei Province, China.
2. Department of Hematopathology, The Second Hospital of Hebei Medical University, Hematology Key Laboratory of Hebei Province, Shijiazhuang 050000, Hebei Province, China.E-mail: ljm315@163.com.
- Publication Type:Journal Article
- Keywords:
acute myeloid leukemia;
drug resistance;
drug-resistant cell;
homologous box gene 1
- MeSH:
Humans;
HL-60 Cells;
Drug Resistance, Neoplasm/genetics*;
Leukemia, Myeloid, Acute;
Doxorubicin/pharmacology*;
Apoptosis;
Cell Proliferation;
Homeodomain Proteins/genetics*
- From:
Journal of Experimental Hematology
2023;31(4):1038-1043
- CountryChina
- Language:Chinese
-
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.
