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作 者:陈汉春[1] public.cs.hn.cn 罗志勇[1] 罗赛群[1] 汤立军[1] 王吉伟[1] 谭孟群[2]
机构地区:[1]湖南医科大学分子生物学研究中心 [2]湖南医科大学血液生理学研究室,湖南长沙410078
出 处:《癌症》2000年第7期627-630,共4页Chinese Journal of Cancer
基 金:国家自然科学基金!39570805
摘 要:目的:探讨羟基脲(hydroxyurea,Hu)及Hu联合粒系-巨噬系集落刺激因子(granulocyticmacrophagecolony-stimulatingfactor,GM-CSF)对慢性粒细胞白血病(chronicmyelogenousleukemia,CML)细胞株K562细胞生长及凋亡相关基因表达的调节效应。方法:以Hu及Hu联合GM-CSF培养K562细胞,采用逆转录-聚合酶链反应(RT-PCR)来分析培养48小时后bcr-abl、bax、c-myc基因表达水平。结果:Hu显著抑制bcr-abl基因表达,促进bax基因表达,但对c-myc基因表达无影响。GM-CSF可部分桔抗Hu对bcr-abl、bax基因表达的调节效应,显著上调c-myc基因表达水平。结论:除直接细胞毒作用外,Hu可通过下调bcr-abl和上调bax基因表达水平而诱导细胞死亡或凋亡。由于GM-CSF有部分持抗化疗药物的效应,故临床上在采用Hu治疗CML患者的同时,宜慎重使用GM-CSF。Objective: To investigate the regulatory effects of hydroxyurea (Hu) and Hu combined with granulocytic macrophage colony-stimulating factor (GM-CSF) on growth and apoptosis-related oncogene expressions in K562 cells.Methods: K562 cells were incubated with Hu or with Hu and GM-CSF collectively. The levels of bcr-abl, bax, c-myc gene expression in the cells following 48 hours culture were analysed by using RT-PCR technique. Results: Hu singificantly suppressed the expression of bcr-abl chimeric gene, and sharply accelerated bax gene expression, but did not affect c-myc gene expression. GM-CSF was able to partially inhibit the regulatory effects of Hu on bcr-abl and bax gene expression, and also significantly upregulated the level of c-myc gene expression. Conclusion: In addition to the direct cytotoxicity, Hu can downregulate the level of bcr-abl chimeric gene expression and upregulate the level of bax gene expression. GM-CSF is capable of enhancing the expression of c-myc gene relating to cell proliferation. GM-CSF should be used cautiously when patients with CML were treated by chemotherapy drugs.
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