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目的:研究甲基化转移酶抑制剂5-杂氮-2’-脱氧胞苷(5-aza-2’-deoxycitydine,5-aza-2dC)对人急性髓系白血病细胞HL-60细胞蛋白质表达谱的影响,探讨5-aza-2dC抗急性髓系白血病作用的机制。方法:采用二维凝胶电泳(2-DE)技术分离5-aza-2-dC处理与未处理HL-60细胞的总蛋白质,PDquest图像分析软件识别差异蛋白质点,基质辅助激光解吸电离飞行时间质谱(MALDI-TOF-MS)鉴定差异蛋白质点。然后采用Western印迹检测差异蛋白质半乳糖凝集素1(Galectin-1)在药物处理与未处理HL-60细胞中的表达水平。结果:建立了5-aza-2dC处理与未处理HL-60细胞蛋白质的2-DE图谱,识别了35个差异表达的蛋白质点,鉴定了27个差异表达的蛋白质,其中包括Galectin-1在内的21个蛋白质在5-aza-2dC处理后的HL-60细胞中表达上调,6个蛋白质表达下调或缺失。Western印迹结果证实Galectin-1在5-aza-2dC处理HL-60细胞中表达上调。结论:21个表达上调蛋白质的编码基因可能是HL-60细胞的甲基化失活基因,它们可能与急性髓系白血病发病以及5-aza-2-dC抗人急性髓系白血病细胞作用有关。
AIM: To investigate the protein expression of 5-aza-2’-deoxycitydine (5-aza-2dC) on human acute myeloid leukemia HL-60 cells Spectrum of the impact of 5-aza-2dC anti-acute myelogenous leukemia mechanism. Methods: The total protein of 5-aza-2-dC-treated and untreated HL-60 cells was separated by two-dimensional gel electrophoresis (2-DE). PDquest image analysis software was used to identify the differential protein spots. The matrix-assisted laser desorption ionization time Differential protein spots were identified by mass spectrometry (MALDI-TOF-MS). Western blotting was then used to detect the expression level of Galectin-1 in drug-treated and untreated HL-60 cells. RESULTS: A 2-DE map of proteins of 5-aza-2dC-treated and untreated HL-60 cells was established, 35 differentially expressed protein spots were identified, and 27 differentially expressed proteins were identified, including Galectin-1 Of the 21 proteins were upregulated in HL-60 cells treated with 5-aza-2dC, and 6 proteins were down-regulated or down-regulated. Western blot results confirmed that Galectin-1 was upregulated in 5-aza-2dC-treated HL-60 cells. CONCLUSION: The 21 genes that overexpress proteins may be the methylation inactivated genes of HL-60 cells, which may be related to the pathogenesis of acute myeloid leukemia and the role of 5-aza-2-dC in anti-human acute myeloid leukemia cells.