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| 组蛋白去乙酰化抑制剂SBHA对急性髓细胞白血病细胞的杀伤作用 | |
| 引用本文： | 徐燕华,杨春梅,钱文斌.组蛋白去乙酰化抑制剂SBHA对急性髓细胞白血病细胞的杀伤作用[J].浙江大学学报(医学版),2012,41(5):491-497. |
| 作者姓名： | 徐燕华 杨春梅 钱文斌 |
| 作者单位： | 1. 浙江理工大学生命科学学院新元医学与生物技术研究所,浙江杭州,310018 2. 浙江大学医学院附属第一医院血液科,浙江杭州,310003 3. 浙江理工大学生命科学学院新元医学与生物技术研究所,浙江杭州310018;浙江大学医学院附属第一医院血液科,浙江杭州310003 |
| 基金项目： | 浙江省自然科学基金杰出青年团队(No.R2090392);浙江省科技厅公益性技术应用研究计划(No.2012C37103)资助项目;浙江省理工大学科研启动基金(No.1016834-Y) |
| 摘 要： | 目的:观察组蛋白去乙酰化抑制剂suberic bishydroxamate( SBHA)对人急性髓系白血病(AML)细胞株的杀伤作用.方法:将不同浓度的SBHA分别作用于对数生长期的AML细胞24 h,MTT比色法检测药物对细胞的生长抑制作用；应用流式细胞术(FACS)检测细胞凋亡率,Westernblot法检测药物处理后Caspase途径和凋亡相关蛋白的改变.结果:SBHA能显著抑制AML细胞株U937ˉ、KG-1及Kasumi-1细胞的生长.AnnexinV-PI双标记法及FACS分析结果证实,SBHA能显著诱导白血病细胞的凋亡,激活Caspase-3、Caspase-9、Caspase-8,下调抗凋亡蛋白Bcl-2及Bcl-xl的表达,下调Survivin、XIAP及cIAP的表达.结论:组蛋白去乙酰化抑制剂SBHA能显著抑制人AML细胞株的增殖、促进其凋亡,对凋亡相关蛋白的调控是其作用机制之一. |
| 关 键 词： | 白血病 髓样 急性/药物疗法 白血病 髓样 急性/病理学 蛋白激酶抑制剂/化学 细胞凋亡/药物作用 肿瘤细胞 培养的 |
Antitumor activity of histone deacetylase inhibitor suberic bishydroxamate on acute myeloid leukemia cell lines |
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| XU Yan-hua , YANG Chun-mei , QIAN Wen-bin.Antitumor activity of histone deacetylase inhibitor suberic bishydroxamate on acute myeloid leukemia cell lines[J].Journal of Zhejiang University(Medical Sciences),2012,41(5):491-497. | |
| Authors: | XU Yan-hua YANG Chun-mei QIAN Wen-bin |
| Institution: | 1,2(1.School of Life Sciences,Xinyuan Institute of Medicine and Biotechnology,Zhejiang Sci-Tech University,Hangzhou 310018,China 2.Department of Hematology,the First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China) |
| Abstract: | Objective: To investigate the effect of histone deacetylase inhibitor suberic bishydroxamate(SBHA) on human acute myeloid leukemia(AML) cell lines.Methods: AML U937,KG-1 and Kasumi-1 cells were treated with SBHA.Cell growth was measured by MTT assay.Apoptosis was determined using flow cytometry.Activation of Caspase pathway and expression of apoptosis regulator proteins were detected by Western blot.Results: SBHA significantly induced growth arrest and apoptosis in U937,KG-1 and Kasumi-1 cells.Enhanced apoptosis was observed in SHBA group evidenced by strong activation of Caspase-9,Caspase-8 and Caspase-3.SHBA treatment resulted in down-regulation of anti-apoptotic protein Bcl-2 and Bcl-xl expression;down-regulated expression of antiapoptotic proteins survivin,XIAP and cIAP was also detected after SBHA treatment.Conclusion: SBHA can effectively kill AML cells by inhibiting cell growth and inducing apoptosis,which is associated with the activation of Caspase pathway and regulation of apoptotic related proteins. |
| Keywords: | Leukemia myeloid acute/drug therapy Leukemia myeloid acute/pathology Histones/analysis Apoptosis/drug effects Tumor cells cultured |
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