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作 者:刘红利[1] 陈燕[1] 李新刚[1] 吴青[1] 谷俊侠[1]
机构地区:[1]华中科技大学同济医学院附属协和医院血液病研究所,武汉市430022
出 处:《中国肿瘤临床》2005年第16期901-905,共5页Chinese Journal of Clinical Oncology
基 金:国家自然科学基金资助(编号:30271672)
摘 要:目的:研究hGCN5(humangeneralcontrolofaminoacidsynthesisprotein5)在Burkkit淋巴瘤细胞株Dau-di中的表达及曲古柳菌素A(TSA)对细胞增殖、凋亡的影响,探讨其抗肿瘤的分子机制。方法:采用MTT法检测细胞增殖,流式细胞仪检测细胞周期和凋亡率,采用免疫细胞化学法和Westernblot观察Daudi细胞hGCN5蛋白的表达。结果:TSA可明显抑制Daudi细胞增殖;TSA(50、100μg/L)使细胞积聚于G0/G1期;TSA(200μg/L)则使细胞周期受抑于S期,而对G2/M期的作用不明显;TSA(200、400μg/L)处理24h可以诱导细胞凋亡;免疫细胞化学和Westernblot结果均显示处理组hGCN5的吸光度比未处理组明显增加(P<0.05)。结论:TSA通过上调HATs家族成员中hGCN5的表达,实现对Daudi细胞的抗增殖作用。Objective: To investigate the effect of TSA (Trichostatin A) regulating hGCN5 (human general control of amino acid synthesis protein 5) in B-NHL cell line Daudi cells, and to study antiproliferation molecular machenism of TSA on B-NHL. Methods: The cell proliferation was measured by MTY assay. The apoptosis rates and cell cycle were determined with flow cytometry. The expression of hGCN5 in treated Daudi cells was determined by immunocytochemistry and Western blot. Results: The proliferation of Daudi cells was decreased in TSA-treated group. Treatment with TSA(200μg/L) and TSA (400μg/L) for 24h, the apoptosis rates of Daudi cells were (14.74±2.04)% and(17.63±1.25)% respectively. The cell cycle was arrested in G0/G1 phase (50, 100μg/L) and in G2/M phase (200μg/L) for 24h. The expression of hGCN5 in Daudi cells was increased in TSA group (400μg/L) for 24h compared with control group by immunocytochemistry and Western blot (P〈0.05). Conclusion: TSA can increase the expression of hGCN5 in Daudi cells and it plays an important role in regulating B-NHL cell line Daudi cells proliferation effects.
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