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曲古菌素A对食管癌细胞系EC1细胞凋亡的影响 被引量:1

Effects of trichostatin A on apoptosis in esophageal carcinoma cell line EC1 cells
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摘要 目的:探讨曲古菌素A(TSA)对食管癌EC1细胞凋亡的影响。方法:用DMSO(对照组)和0.3、0.5及1.0μmol/L的TSA处理EC1细胞24 h,用Annexin V-FITC和PI双染色,流式细胞仪检测4组细胞的凋亡率,West-ern Blot检测4组细胞中Bax及Bcl-2表达的变化。结果:对照组、0.3、0.5及1.0μmol/L TSA组作用24 h后,EC1细胞凋亡率分别为(2.18±0.37)%、(2.96±0.34)%、(7.41±1.01)%和(14.03±1.23)%,Bax蛋白表达水平分别为(0.42±0.23)、(0.45±0.11)、(1.16±0.28)和(1.89±0.30),Bcl-2蛋白表达水平分别为(1.15±0.14)、(1.11±0.15)、(0.59±0.06)和(0.40±0.07),4组间3指标差异均有统计学意义(F=211.96,25.12和33.68,P均<0.001),随TSA作用浓度的增加,EC1细胞凋亡率、Bax蛋白表达均增加,Bcl-2表达减少。结论:一定剂量的TSA可以诱导EC1细胞凋亡,凋亡的发生可能与Bax表达增加和Bcl-2表达减少有关。 Aim: To explore the effects of trichostatin A on apoptosis in EC1 cells. Methods:EC1 cells at logarithmic growth phase were treated with O. 3 μmol/L, 0.5 μmol/L and 1.0 μmol/L TSA for 24 h, the cells were stained with Annexin V-FITC and PI for analyzing apoptosis by flow cytometry, the expressions of Bax and Bcl-2 were investigated with Western Blot. Cells treated with DMSO were the control. Results: Apoptosis rates of O. 3 μmol/L,0.5 μmol/L, 1.0 μmol/L trichosta- tin A groups and the control group were (2.96 -±0.34)% ,(7.41 ±1.01)% , (14.03 ±1.23)% and (2.18 ±0.37)% ;the Bax expression level was (0.45 ± 0.11 ) , ( 1.16 ± 0.28 ) , ( 1.89 ± 0.30) and (0.42 ± 0.23 ) ; the Bcl-2 expression level was (1.11 ±0.15),(0.59±0.06),(0.40±0.07), and (1.15 ±0.14). There were significant differences in the 3 indexes among the 4 groups (F = 211.96,25.12, and 33.68, all P 〈 O. 001 ). Apoptosis rates and the Bax expression level increased and the Bel-2 expression level decreased with the increase of the dosage of TSA. Conclusion : TSA is able to induce apoptosis of esophageal carcinoma cell line EC1 cells partly through the regulation of the expression of Bax and Bcl-2.
出处 《郑州大学学报(医学版)》 CAS 北大核心 2010年第2期180-182,共3页 Journal of Zhengzhou University(Medical Sciences)
基金 教育部科技研究重大项目207150
关键词 曲古菌素A 细胞凋亡 食管癌 BAX BCL-2 EC1细胞 trichostatin A apoptosis esophageal carcinoma Bax Bcl-2 EC1 cell
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参考文献9

  • 1Marks PA, Miller T, Richon VM. Histone deaeetylases[ J]. Curr Opin Pharmacol, 2003,3 ( 4 ) : 344.
  • 2Habold C, Poehlmann A, Bajbouj K, et al. Trichostatin A causes p53 to switch oxidative-damaged colorectal cancer cells from cell cycle arrest into apoptosis [ J]. J Cell Mol Med,2008 ,12(2) :607.
  • 3Insinga A, Monestiroli S, Ronzoni S, et al. Inhibitors of histone deacetylases induce tumor-selective apoptosis through activation of the death receptor pathway [ J]. Nat Med, 2005,11(1) :71.
  • 4Zhao LY, Niu Y, Santiago A, et al. An EBF3-mediated transcriptional program that induces cell cycle arrest and apoptosis [ J ]. Cancer Res, 2006,66 ( 19 ) :9 445.
  • 5Kang MR, Kang JS, Han SB, et al. A novel δ-lactam-based histone deacetylase inhibitor, KBH-A42,induces cell cycle arrest and apoptosis in colon cancer cells [ J ]. Biochem Pharmacol,2009,78 ( 5 ) :486.
  • 6李云龙,邹小明,袁友萍,尤立光,刘志勇,高鹏,杨春发.曲古菌素A对胃癌细胞系BGC-823组蛋白H4乙酰化水平及细胞凋亡的作用[J].肿瘤学杂志,2008,14(8):654-656. 被引量:2
  • 7Woo HJ,Lee SJ, Choi BT, et al. Induction of apoptosis and inhibition of telomerase activity by trichostatin A, a histone deacetylase inhibitor, in human leukemic U937 cells [ J ]. Exp Mol Pathol,2007,82( 1 ) :77.
  • 8Subramanian C,Opipari AW Jr, Bian X, et al. Ku70 acetylation mediates neuroblastoma cell death induced by histone deacetylase inhibitors [ J]. Proc Natl Acad Sci USA, 2005,102(13) :4 842.
  • 9Ahn MY, Lee J, Na YJ, et al. Mechanism of apicidin-induced cell cycle arrest and apoptosis in Ishikawa human endometrial cancer cells [ J]. Chem Biol Interact, 2009, 179(2/3) :169.

二级参考文献12

  • 1周玉美,王林,钱俊杰,孙志贤.组蛋白去乙酰化酶抑制剂的构效关系研究进展[J].解放军药学学报,2006,22(3):206-209. 被引量:7
  • 2洪振亚,易莉莎,苗新宇,卢运萍,周剑锋,刘文励.应用基因芯片分析曲古菌素A促人白血病细胞株Molt-4凋亡的机制[J].癌症,2006,25(8):946-953. 被引量:6
  • 3Dhordain P, Lin RJ, Quief S, et al. The LAZ3(BCL-6) oncoprotein recruits a SMRT/mSIN3A/histone deaeetylase containing complex to mediate transcriptional repression [J]. Nucleic Acids Res, 1998, 26(20):4645-4651.
  • 4Marks PA, Richon VM, Rifkind RA. Histone deacetylase inhibitors as new cancer drugs[J]. Curt Opin Oncol, 2001, 13(6):477-483.
  • 5Duan H, Heckman CA, Boxer LM. Histone deacetylase inhibitors down-regulate bcl-2 expression and induce apoptosis in t(14;18) lymphomas[J]. Mol Cell Biol, 2005, 25(5): 1608-1619.
  • 6Roy S, Packman K, Jeffrey R, et al. Histone deacetylase inhibitors differentially stabilize acetylated p53 and induce cell cycle arrest or apoptosis in prostate cancer cells [J]. Cell Death Differ, 2005, 12(5):482-491.
  • 7Wang J, Saunthararajah Y, Redner RL, et al. Inhibitors of histone deacetylase relieve ETO-mediated repression and induce differentiation of AML1-ETO leukemia cells [J]. Cancer Res, 1999, 59(12):2766-2769.
  • 8Chen CS, Weng SC, Tseng PH, et al. Histone acetylation- independent effect of histone deacetylase inhibitors on Akt through the reshuffling of protein phosphatase 1 complexes[J]. J Biol Chem, 2005, 280(46):38879-38887.
  • 9Bartova E, Pachernik J, Harnicarova A, et al. Nuclear levels and patterns of histone H3 modification and HP1 proteins after inhibition of histone deacetylases[J]. J Cell Sci, 2005, 118(Pt 21):5035-5046.
  • 10Takakura M, Kyo S, Sowa Y, et al. Telomerase activation by histone deacetylase inhibitor in normal cells[J]. Nucleic Acids Res, 2001, 29(14):3006-3011.

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  • 1方建国,丁水平,田庚元.枸杞多糖药理作用与临床应用[J].医药导报,2004,23(7):484-485. 被引量:78
  • 2Marks PA, Miller T, Richon VM. Histone deacetylases [ J]. CurrOpin Pharmacol, 2003,3 ( 4 ) : 344.
  • 3Habold C, Poehlmann A, Bajbouj K, et al. Trichostain A causes p53 to switch oxidative - damaged colorectal cancer ceils from cell cycle arrest into apoptosis[ J]. Cell Mol Med ,2008,12 (2) :607.
  • 4Zhao LY, Niu Y, Santiago A, et al. Inhibitors of histone deacetylases induce tumor - selective apoptosis through activation of the death receptor pathway [ J ]. Nat Med, 2005,11 ( 1 ) :71.

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