泛素相关蛋白1基因与肿瘤抑制基因p16在急性白血病中的表达研究

Expression of Ubiqutin Associated Protein 1 Gene and Tumor-suppressor Gene p16 in Acute Leukemia

为了探讨泛素相关蛋白1(UBAP1)基因和肿瘤抑制基因(p16)在急性白血病中的表达水平及二者的相关性,采用实时荧光定量PCR技术检测68例急性白血病患者和22例对照者骨髓细胞中ubap1基因和p16基因的mRNA的表达水平。结果发现,在急性白血病中ubap1基因呈高表达,p16基因呈低表达,与对照组相比较有显著性差异(p<0.01)。然而,进一步分组比较发现,ubap1基因仅在成人急性髓系白血病的M4和M5亚型中的表达有统计学意义(p<0.05),p16基因除成人FAB分型的M1和M2亚型外,其余组差异均有统计学意义(p<0.05);而ubap1基因和p16基因的mRNA表达水平在染色体预后分组间差异无统计学意义(p>0.05)。ubap1基因和p16基因的表达水平在对照组中呈显著负相关(r=-0.827,p<0.01),在病例组中无相关性(r=0.065,p>0.05)。结论:ubap1基因高表达与p16基因低表达可能同时参与急性白血病的发病,其中ubap1基因高表达主要影响AML中M4和M5亚型的发病,这一发现为进一步探讨急性白血病发病机制及靶向治疗提供重要的理论依据。

In order to investigate the expression and the relationship of ubiqutin associated protein 1（ubap1） gene and tumor-suppressor gene p16 in acute leukemia,68 cases of acute leukemia and 22 control cases were selected in this experiment,FQ-PCR technique was used to detect the mRNA expression level of ubap1 gene and p16 gene in their bone marrow cells.The results showed that as compared with the control group,the ubap1 gene in acute leukemia group highly expressed（p0.01）,while the p16 gene lowly expressed（p0.01）.But grouping of patients according to FAB revealed that as compared with the control group,the ubap1 gene expression displayed statistical difference only in M4 and M5 of adult AML（p0.05）,while the p16 gene expression in all groups of adult AML showed significant difference（p0.05） except M1 and M2.In addition to this,the ubap1 gene and p16 gene mRNA expression in AL was not relate with chromosome abnormality（p0.05）.A negative correlation（r=-0.827,p0.01） was found between the ubap1 gene and p16 gene mRNA expressions in the control group.It is concluded that the upregulation of ubap1 gene expression mainly and the downregulation of p16 gene expression mainly may simultaneously participate in the pathogenesis of acute leukemia.High expression of ubap1 gene influences the M4 and M5 subtypes in AML.This discovery provides important theoretical basis for the further investigation of pathogenesis and targeting therapy of AL.