中文摘要：

背景与目的：BCR／ABL诱导多聚胞嘧啶结合蛋白E2[poly（rC）-binding protein E2．hnRNP E2]的异常表达在慢性粒细胞白血病（chronic myeloid leukemia，CML）急变中起着重要作用。本研究探讨hnRNP E2诱骗RNA（decoy RNA）对人白血病细胞K562增殖的影响，并初步探讨其可能的分子机制。方法：构建能转录出hnRNP E2诱骗RNA的质粒载体,将其经阳离子脂质体介导转染K562细胞，用G418筛选出稳定表达的细胞，台盼蓝法检测细胞的增殖能力，流式细胞仪分析细胞周期，并用RT-PCR和Western blot方法检测下游CCAAT增强子结合蛋白α（CCAAT／enhancer-binding proteinα，C／EBPα）和c-myc的表达。结果：稳定表达诱骗RNA的K562细胞增殖受抑，增殖抑制率为（62．73±12．92）％；细胞周期阻滞于S期[稳定表达诱骗RNA细胞组（55．59±4．67）％，对照组（44．70±4．21）％，P〈0．05]；C／EBPα mRNA无改变，但在蛋白水平42 ku-C／EBP仅表达升高了（49．72±5．58）％；c-myc mRNA下降了（58．27±7．23）％，蛋白水平降低了（57．26±6．52）％。结论：hnRNP E2诱骗RNA能抑制K562细胞的增殖,其机制可能与诱骗RNA阻断hnRNP E2和C／EBPα mRNA的结合后，引起42ku-C／EBPα表达升高有关。

英文摘要：

BACKGROUND ＆ OBJECTIVE. The abnormal expression of poly （rC）-binding protein E2 （hnRNP E2） induced by BCR/ABL plays an important role in blast crisis of chronic myeloid leukemia （CML）. The present study was to investigate the effect of hnRNP E2 decoy RNA on the cell proliferation in K562 leukemia cells, and further elucidate the possible underlying mechanisms. METHODS： Decoy hnRNP E2 plasmid was constructed and transfected into K562 cells using cationic liposome. Stably transfected cells were selected with G418. The cell proliferation rate was determined by cell growth curve using trypan blue staining, and the cell cycle was analyzed by flow cytometry. The changes of CCAAT/enhancerbinding protein α （C/EBP α） and c-Myc gene expression were detected by reverse transcription polymerase chain reaction （RT-PCR） and Western blot. RESULTS：The proliferation rate of stably transfected K562 cells was inhibited by （62.73±12.92）%. The cell cycle was arrested at S phase [stably transfected K562 cell group： （55.59±4.67）%,control group： （44.70± 4.21）%, P〈0.05]; C/EBPα mRNA level remained unchanged. However the 42 ku-C/EBPα protein expression was elevated by （49.72±5.58）%; c-Myc mRNA and protein expression was inhibited by（58.27±7.23）% and （57.26± 6.52）%, respectively. CONCLUSlON：HnRNP E2 decoy RNA could inhibit the proliferation of K562 cells, and this may be caused by the blockage of the binding between hnRNP E2 and C/EBPα mRNA and subsequent elevation of 42 ku-C/EBPα by decoy RNA.