PI3K/AKT信号通路在急性白血病中调控机制的初步研究

摘要

本研究探讨PI3 K/AKT通路中的PTEN、CCND1、mTOR、RICTOR、FOX01基因在急性髓系白血病(AML)、急性淋巴细胞白血病(ALL)患者中与正常人中表达的差异,以期查明PI3 K/AKT通路在白血病中是否存在通路失调.随机收集16例骨髓标本,其中白血病12例(AML 6例,ALL 6例),正常骨髓标本4例.用实时定量RT-PCR方法检测PI3K/AKT通路中的PTEN、CCND1、mTOR、RICTOR、FOX01基因的表达变化；以管家基因GAPDH为内参,按2 -△△Ct法计算目的基因相对表达量.结果表明:PTEN、mTOR、RICTOR在AML、ALL中总体呈低表达趋势,PTEN在12例标本中有10例低表达,mTOR在12例标本中9例低表达,RICTOR在12例标本中7例低表达；FOXO1,CCND1在AML、ALL中则呈高表达趋势,FOXO1在12例标本中有9例高表达,CCND1在12例标本中7例高表达.结论:PI3K/AKT信号通路基因在白血病细胞中被激活.%This study was aimed to analyze the expression profiles of PI3K/AKT signaling pathway genes from bone marrow samples of AML and ALL patients and normal samples. AML, ALL and normal bone marrow samples were collected from 6 AML, 6 ALL patients and 4 normal persons. The expression of PI3K/AKT signaling pathway genes including PTEN, CCND1, mTOR, RICTOR, FOXO1 were detected by real-time fluorescent quantification RT-PCR while GAPDH gene expression was used as an internal reference. The relative gene expression level was calculated by the method of the 2 ~AAC1. The results showed that the gene expression profiles were different between normal and leukemic groups. PTEN, mTOR and RICTOR expression levels were down-regulated, while FOXO1 and CCND1 levels were up-regulated in AML and ALL. PTEN was down-regulated in 10 out of the 12 samples; mTOR was down-regulated in 9 out of the 12 samples; RICTOR was down-regulated in 7 out of the 12 samples; FOXO1 was up-regulated in 9 out of the 12 samples and CCND1 was up-regulated in 7 out of the 12 samples. It is concluded that PI3K/AKT signal pathway is activated in both AML and ALL leukemic cells.