{"title":"[Effect of Selinexor on Proliferation and Apoptosis of Acute Myeloid Leukemia Kasumi-1 Cells].","authors":"Lu-Hui Lin, Sun-Qiao Gao, Xu-Qiao Mei, Da-Yi Lin, Yi-Feng Chen, Su-Dan Lin, Li-Hong Zhuang, Cong-Meng Lin","doi":"10.19746/j.cnki.issn.1009-2137.2024.04.017","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of selinexor, a inhibitor of nuclear export protein 1 (XPO1) on the proliferation inhibition and apoptosis of Kasumi-1 cells in acute myeloid leukemia (AML).</p><p><strong>Methods: </strong>MTS method was used to detect the inhibitory effect of different concentrations of selinexor on the proliferation of Kasumi-1 cells at different time points. The apoptosis rate and cell cycle changes after treatment with different concentration of selinexor were detected by flow cytometry.</p><p><strong>Results: </strong>Selinexor inhibited the growth of Kasumi-1 cells at different time points in a concentration-dependent manner (<i>r</i> <sub>24 h</sub>=0.7592, <i>r</i> <sub>48 h</sub>=0.9456, and <i>r</i> <sub>72 h</sub>=0.9425). Selinexor inhibited Kasumi-1 cells growth in a time-dependent manner (<i>r</i> =0.9057 in 2.5 μmol/L group, <i>r</i> =0.9897 in 5 μmol/L group and <i>r</i> =0.9994 in 10 μmol/L group). Selinexor could induce apoptosis of Kasumi-1 cells in a dose-dependent manner (<i>r</i> =0.9732), and the apoptosis of Kasumi-1 cells was more obvious with the increase of drug concentration. The proportion of G<sub>0</sub>/G<sub>1</sub> phase was significantly increased and the proportion of S phase was significantly decreased after the treatment of Kasumi-1 cells by selinexor. With the increase of drug concentration, the proportion of Kasumi-1 cells cycle arrest in G<sub>0</sub>/G<sub>1</sub> phase was increased and the cell synthesis was decreased.</p><p><strong>Conclusion: </strong>Selinexor can promote the death of tumor cells by inhibiting Kasumi-1 cells proliferation, inducing apoptosis and blocking cell cycle.</p>","PeriodicalId":35777,"journal":{"name":"中国实验血液学杂志","volume":"32 4","pages":"1085-1090"},"PeriodicalIF":0.0000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"中国实验血液学杂志","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.19746/j.cnki.issn.1009-2137.2024.04.017","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To investigate the effects of selinexor, a inhibitor of nuclear export protein 1 (XPO1) on the proliferation inhibition and apoptosis of Kasumi-1 cells in acute myeloid leukemia (AML).
Methods: MTS method was used to detect the inhibitory effect of different concentrations of selinexor on the proliferation of Kasumi-1 cells at different time points. The apoptosis rate and cell cycle changes after treatment with different concentration of selinexor were detected by flow cytometry.
Results: Selinexor inhibited the growth of Kasumi-1 cells at different time points in a concentration-dependent manner (r24 h=0.7592, r48 h=0.9456, and r72 h=0.9425). Selinexor inhibited Kasumi-1 cells growth in a time-dependent manner (r =0.9057 in 2.5 μmol/L group, r =0.9897 in 5 μmol/L group and r =0.9994 in 10 μmol/L group). Selinexor could induce apoptosis of Kasumi-1 cells in a dose-dependent manner (r =0.9732), and the apoptosis of Kasumi-1 cells was more obvious with the increase of drug concentration. The proportion of G0/G1 phase was significantly increased and the proportion of S phase was significantly decreased after the treatment of Kasumi-1 cells by selinexor. With the increase of drug concentration, the proportion of Kasumi-1 cells cycle arrest in G0/G1 phase was increased and the cell synthesis was decreased.
Conclusion: Selinexor can promote the death of tumor cells by inhibiting Kasumi-1 cells proliferation, inducing apoptosis and blocking cell cycle.