Effect of Scutellarin on Proliferation of Acute Myeloid Leukemia Cells and Its Related Mechanism.
10.19746/j.cnki.issn.1009-2137.2023.02.008
- Author:
Jun CHEN
1
;
Yi-Feng CAI
2
,
3
;
Min SHAO
1
;
Hui CONG
4
Author Information
1. Department of Blood Transfusion, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
2. Department of Blood Transfusion, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China .E-mail:caiyf996@
3. com.
4. Department of Clinical Laboratory, The Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China.
- Publication Type:Journal Article
- Keywords:
JAK2/STAT3 signaling pathway;
acute myeloid leukemia;
cell cycle;
cell proliferation;
scutellarin
- MeSH:
Humans;
Apoptosis;
Signal Transduction;
Leukemia, Myeloid, Acute;
HL-60 Cells;
Cell Proliferation;
Cell Line, Tumor
- From:
Journal of Experimental Hematology
2023;31(2):358-363
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of scutellarin (SCU) on proliferation, cell cycle and apoptosis of acute myeloid leukemia (AML) cells and its related molecular mechanism.
METHODS:Human AML HL-60 cells were cultured in vitro. The cells were treated with SCU at the concentration of 0, 2, 4, 8, 16, 32, 64 μmol/L, and the inhibition rate of cell proliferation was detected by CCK-8 method. Then HL-60 cells were treated with SCU at the concentration of 4, 8, 16 μmol/L, and the negative control group (NC group) was set. The cell cycle distribution and apoptosis were detected by flow cytometry, and the expression of cell cycle, apoptosis and JAK2/STAT3 pathway related proteins were detected by Western blot.
RESULTS:SCU significantly inhibited the proliferation of HL-60 cells in a concentration- and time-dependent manner(r =0.958,r =0.971). Compared with NC group, the proportion of cells in G0/G1 phase and apoptosis rate of HL-60 cells in 4, 8, 16 μmol/L SCU group were significantly increased, and the proportion of cells in S phase was significantly decreased (P <0.05). The relative protein expression levels of p21, p53, caspase-3 and Bax were significantly increased, while the relative protein expression levels of CDK2, cyclin E and Bcl-2 were significantly decreased (P <0.05). The ratio of p-JAK2/JAK2 and p-STAT3/STAT3 were significantly decreased (P <0.05). The changes of above-mentioned indexes were concentration dependent.
CONCLUSION:SCU can inhibit the proliferation of AML cells, induce cell cycle arrest and apoptosis, and its mechanism may be related to the regulation of JAK2/STAT3 signaling pathway.
