中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
13期
890-893
,共4页
孟月生%魏蓉%艾工文%孟秀琴%张燕香
孟月生%魏蓉%艾工文%孟秀琴%張燕香
맹월생%위용%애공문%맹수금%장연향
LYL1%LMO2%白血病,髓系
LYL1%LMO2%白血病,髓繫
LYL1%LMO2%백혈병,수계
LYL1%LMO2%Leukemia,myeloid
目的 探讨转录因子LMO2与LYL1在髓系白血病细胞的表达、相互作用及意义.方法 荧光实时定量聚合酶链反应、基因转染与免疫共沉淀实验等.结果 LMO2在51.1%的未缓解急性髓系自血病(AML)患者表达增强,LYL1在62.2%的AML患者表达增强,二者共同高表达的患者比例为31.1%,表达水平有正相关性.基因转染实验显示LMO2与LYL1的表达相互激活.应用免疫共沉淀证明髓系白血病细胞中LMO2-LYL1复合物的存在.结论 LMO2与LYL1在白血病细胞的表达异常和相互作用可能是引起髓系造血细胞增殖分化异常的重要因素.
目的 探討轉錄因子LMO2與LYL1在髓繫白血病細胞的錶達、相互作用及意義.方法 熒光實時定量聚閤酶鏈反應、基因轉染與免疫共沉澱實驗等.結果 LMO2在51.1%的未緩解急性髓繫自血病(AML)患者錶達增彊,LYL1在62.2%的AML患者錶達增彊,二者共同高錶達的患者比例為31.1%,錶達水平有正相關性.基因轉染實驗顯示LMO2與LYL1的錶達相互激活.應用免疫共沉澱證明髓繫白血病細胞中LMO2-LYL1複閤物的存在.結論 LMO2與LYL1在白血病細胞的錶達異常和相互作用可能是引起髓繫造血細胞增殖分化異常的重要因素.
목적 탐토전록인자LMO2여LYL1재수계백혈병세포적표체、상호작용급의의.방법 형광실시정량취합매련반응、기인전염여면역공침정실험등.결과 LMO2재51.1%적미완해급성수계자혈병(AML)환자표체증강,LYL1재62.2%적AML환자표체증강,이자공동고표체적환자비례위31.1%,표체수평유정상관성.기인전염실험현시LMO2여LYL1적표체상호격활.응용면역공침정증명수계백혈병세포중LMO2-LYL1복합물적존재.결론 LMO2여LYL1재백혈병세포적표체이상화상호작용가능시인기수계조혈세포증식분화이상적중요인소.
Objective To explore the expression of the transcription factors LMO2 and LYL1 and the interaction between these 2 factors in myeloid leukemia cells and to analyze the significance thereof in leukemogenesis. Methods Samples of peripheral blood and bone marrow were collected form 51 AML patties, and 5 normal bone marrow donors to isolate mononuclear cells (MNCs) with high percentage of CD34 (+) cells. Western blotting (WB) was used to detect the protein expression of LMO2 and LYL1 in the cells. Human myeloid leukemia cells of the line K562 were cultured and transfected with pcDNA3-LMO2, plasmid containing LMO2, pcDNA3-LYL1, plasmid containing LYL1, or pcDNA-GFP, blankplasmid containing green fluorescent protein. RT-PCR was used to detect the mRNA expression of LMO2 and LYL1. Co-immunoprecipitation (co-IP) and WB were used to detect the binding protein of LMO2 and LYL1. Results The MNCs of 51.1% of the patients with acute myeloblastic leukemia (AML) without remission expressed higher levels of LMO2, the MNCs of 62.2% of the AML patients expressed higher levels of LYL1, and the MNCs of 31.1% of those expressed both. The K562 cells transfected with pcDNA3-LMO2 showed higher mRNA and protein expression levels of both LMO2 and LYL1, and the K562 cells transfected with pcDNA3-LYL1 showed higher mRNA and protein expression levels of both LYL1 and LMO2 too, as indicated by RT-PCR and WB, which suggested that the expression of LMO2 and the expression of LYL1 stimulated each other in the myeloid leukemia cells. Co-IP assay detected the presence of LMO2-LYL1 complex in those cells. Conclusion The abnormal expression and protein interaction of LMO2 and LYL1 may play a role in the abnormal proliferation and differentiation of myeloid hematopoietic cells.