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曲古菌素A对人胃癌SGC-7901细胞凋亡及其DAPK1基因表达的影响 被引量：1

Effects of trichostatin on apoptosis and expression of DAPK1 gene in human gastric cancer SGC-7901 cells
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摘要 目的探讨曲古菌素A(TSA)体外抑制人胃癌SGC-7901细胞凋亡及其死亡相关蛋白激酶1(DAPK1)基因表达的影响。方法体外培养的胃癌细胞以不同浓度的TSA(37.5、150、600ng/ml)处理后,用AnnexinⅤ/PI检测细胞凋亡率,RT-PCR、Westernblot分别检测DAPK1mRNA和蛋白表达水平。结果 AnnexinⅤ/PI检测发现,不同浓度TSA可显著诱导SGC-7901细胞凋亡,并呈浓度及时间依赖性(P<0.05);TSA干预前SGC-7901细胞DAPK1mRNA和蛋白表达水平很低,不同浓度TSA处理SGC-7901细胞DAPK1mRNA和蛋白表达水平明显上调,呈溶度及时间依赖性(P<0.05)。结论 TSA诱导SGC-7901细胞凋亡可能与DAPK1基因的低乙酰化状态逆转有关。 Objective To study the effects of trichostatin on apoptosis and expression of death-associated protein kinase-1（DAPK1） gene in human gastric SGC-7901 cells.Methods SGC-7901 cells were treated with TSA at different concentrations（37.5,150,600 ng/ml）.The apoptosis of the cells was evaluated by AnnexinV/PI.The expressions of DAPK1 mRNA and protein were detected with RT-PCR and Western blot.Results AnnexinV/PI showed that the apoptosis rate in SGC-7901 cell went up significantly in a dose-and time-dependent manner（P0.05）.The mRNA and protein expression of DAPK1 gene were detected in a very low level in the gastric cancer SGC-7901 cells before treatment,which were increased in a dose-and time-dependent manner after treaded with TSA at different concentrations and times（P0.05）.Conclusion TSA-induced apoptosis of gastric cancer SGC-7901 cells may be related to the reverse of low histone acetylation level.
作者 程海燕 陈卫昌 严苏
机构地区 苏州大学附属第一医院消化病科
出处 《江苏医药》 CAS CSCD 北大核心 2010年第9期1068-1070,共3页 Jiangsu Medical Journal
关键词 曲古菌素A SGC-7901细胞 死亡相关蛋白激酶1基因 Trichostatin SGC-7901 cell Death-associated protein kinase 1（DAPK1）
分类号 R735 [医药卫生—肿瘤]
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参考文献7

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同被引文献8

  • 1Gregoretti IV, Lee YM, Goodson HV. Molecular evolution of the historte deacetylase family: functional implications of phylogenetic analysis[J]. J Mol Biol,2004,338(1):17-31.
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  • 7Oehme I,Deubzer HE,Wegener D,et al. Histone deacetylase 8 in neuroblastoma tumorigenesis[J]. Clin Cancer Res, 2009,15 (1) : 91-99.
  • 8Murakami K, Matsubara H, Hoshino I, et al. CHAP31 induces apoptosis only via the intrinsic pathway in human esophageal cancer cells[J]. Oncology,2010,78(1):62-74.

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江苏医药
2010年 第9期

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