摘要
目的:分析急性髓系白血病(AML)中三基序蛋白58(tripartite-motif protein 58,TRIM58)基因启动子甲基化水平与其mRNA表达的关系,探讨TRIM58基因在AML中的表达调控。方法:分别用亚硫酸氢盐修饰后PCR、实时荧光定量PCR技术检测原代CD34^(+)和CD34^(-)AML细胞以及白血病细胞株KG1a、K562中TRIM58基因启动子甲基化状态和TRIM58mRNA表达情况。结果:AML患者CD34^(+)细胞TRIM58基因mRNA表达下调10例,CD34^(-)细胞TRIM58基因mRNA表达下调12例,TRIM58基因启动子甲基化水平与正常对照比较存在统计学差异(P<0.05);KG1a及K562细胞株中TRIM58mRNA表达下调,经地西他滨处理后TRIM58mRNA表达上调。结论:AML细胞中TRIM58mRNA表达下调,可能与其启动子甲基化状态具有相关性。
Objective:To analyze the relationship between the promoter methylation status of Tripartite-motif protein58(TRIM58)and its mRNA expression level in acute myeloid leukemia(AML),and to explore the expression and regulation of TRIM58 in AML. Methods:The bisulfite sequencing PCR(BSP)and quantitative real-time PCR(qPCR)technologies were used to detect the promoter methylation status and expression levels of TRIM58 mRNA in primary CD34^(+) and CD34^(-)AML cells and the AML cell lines KG1a and K562were determined. Results:The expression of TRIM58 mRNA in CD34^(+) cells was down-regulated in10AML patients,while that in CD34^(-)cells was down-regulated in12cases. Differences in the promoter methylation level of TRIM58 were statistically significant between AML group and normal control group(P< 0.05). Additionally,the expression of TRIM58 mRNA was down-regulated in cell lines KG1a and K562,and up-regulated after decitabine treatment. Conclusion:The down-regulation of mRNA expression of TRIM58 in AML cells may be related to its promoter methylation status.
作者
杜成坎
江月
卢莹
杨雪
DU Cheng-Kan;JIANG Yue;LU Ying;YANG Xue(Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China;The second Afiliated Hospital of Dalian Medical University,Dalian 116023,Liaoning Province,China;Xinhua Hospital Afiliated to Shanghai Jiao Tong University School of Medicine,Shanghai 200092,China;Shanghai Ninth People's Hospital Afiliated to Shanghai Jiao Tong University School of Medicine,Shanghai 200011,China)
出处
《中国实验血液学杂志》
CAS
CSCD
北大核心
2022年第5期1354-1360,共7页
Journal of Experimental Hematology
基金
国家自然基金面上项目(81770146)。
