Inducing Effect of Decitabine on Apoptosis of KMS-18 Myeloma Cells and Its Mechanism.
10.19746/j.cnki.issn.1009-2137.2019.04.025
- Author:
Xiao-Ning WANG
1
;
Mei ZHANG
2
;
Peng-Cheng HE
3
Author Information
1. Department of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China.
2. Department of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China,E-mail: zhangmei@medmail.com.cn.
3. Department of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China,E-mail: hepc@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Line, Tumor;
Cell Proliferation;
DNA Methylation;
Decitabine;
Humans
- From:
Journal of Experimental Hematology
2019;27(4):1149-1153
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of decitabine on proliferation and apoptosis of multiple myeloma KMS-18 cells and its possible mechanism.
METHODS:CCK-8 was used to detect cell proliferation, flow cytometry was used to detect the changes of apoptosis, real-time quantitative PCR was used to detect the expression of P53 gene mRNA in myeloma KMS-18 cells, and MSP assay was used to detect the methylation status of P53 gene promoter.
RESULTS:The proliferation inhibition and apoptosis of KMS-18 cells significantly increased after treatment by decitabine (P＜0.05). The expression of P53 mRNA increased in KMS-18 cells after treatment of decitabine (P＜0.05). The methylation status of the P53 gene promoter in KMS-18 cells could be partially reversed by decitabine.
CONCLUSION:Decitabine can inhibit the proliferation of KMS-18 cells and induce their apoptosis, its mechanism ralates with partially reversing the methylation of P53 gene promoter in KMS-18 cells.
