[Inducing Effect of Decitabine on Apoptosis of KMS-18 Myeloma Cells and Its Mechanism]

To investigate the effect of decitabine on proliferation and apoptosis of multiple myeloma KMS-18 cells and its possible mechanism.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.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.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.地西他滨诱导多发性骨髓瘤KMS-18细胞凋亡及其机制研究.研究地西他滨对多发性骨髓瘤KMS-18细胞的抑制增殖及诱导凋亡的作用及其可能机制.采用CCK-8法检测不同浓度地西他滨干预后KMS-18细胞增殖抑制率；流式细胞术检测地西他滨干预的细胞凋亡变化；实时荧光定量PCR检测地西他滨干预前、后P53基因mRNA表达水平；MSP法检测地西他滨干预前后P53基因启动子甲基化的状态.地西他滨干预后KMS-18细胞增殖抑制率呈时间及浓度依赖性增加（r =0.9790，P＜0.05）；干预后细胞凋亡率显著增加，差异有统计学意义（P＜0.05）；地西他滨干预后KMS-18细胞P53基因mRNA表达增加（P＜0.05）；地西他滨可以部分逆转KMS-18细胞P53基因启动子甲基化状态.地西他滨可抑制细胞增殖，并诱导其凋亡，与其部分逆转KMS-18细胞P53基因启动子甲基化有关.