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辛二酰苯胺异羟肟酸(SAHA)对乳腺癌细胞增殖影响的动物实验研究 被引量:4

Effect of Histone Deacetylase Inhibitor SAHA on Breast Cancer Cell in Animal Mode
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摘要 目的探讨组蛋白去乙酰化酶抑制剂SAHA对乳腺癌细胞株增殖周期的影响。方法饲养Balb/c-nu/nu雌性裸鼠,细胞悬液皮下注射法构建人乳腺癌细胞株MCF-7裸鼠移植瘤模型,随机分为6组,经尾静脉注射不同剂量的SAHA,获取血细胞分析、血脂、肝功能、肾功能、裸鼠体重、瘤重等数据,计算肿瘤生长抑制率、移植瘤的体积,进行统计分析。结果不同剂量的SAHA作用于乳腺癌荷瘤裸鼠后,通过比较肿瘤体积及抑瘤率均显示出疗效,在0.10~0.42 mg/kg剂量范围内,SAHA的治疗效应呈现剂量依赖关系;其作用后导致血清胆红素和谷丙转氨酶水平升高,对红细胞、白细胞及血小板计数、尿素氮、肌酐水平影响不明显。结论 SAHA是乳腺癌细胞增殖抑制剂,其抑制效应有一定的量效关系;其对机体副作用较小。 Objective To study the effect of histone deacetylase inhibitor SAHA on breast cancer cell in animal mode.Methods MCF-7 breast cancer nude mouse model was constructed by hypodermic injection of breast cancer cell suspension,and different dose of SAHA was given through tail vein injection.The blood was then taken to analyze the blood fat,the liver and the kidney function,and the body weight and wet weight of tumor were measured.The tumor growth inhibition rate and tumor volume were analyzed by SPSS 10.0.Results Curative effect was observed in all the dose level group of SAHA.Within the 0.10~0.42 mg/kg dosage range,the SAHA treatment effect presented the dose-dependent relations,but no additional curative effect was observed when the dose increased from 0.42 mg/kg to 0.84 mg/kg;Increase of serum glutamic-pyruvic transaminase and bilirubin was observed after SAHA treatment,but SAHA had no effects on the kidney function,blood count and cholesterol.Conclusion SAHA is a powerful and dose-dependant histone deacetylase inhibitor for breast cancer cell with few side effects.
出处 《实用癌症杂志》 2011年第3期221-225,共5页 The Practical Journal of Cancer
基金 中国人事部留学人员科技活动项目择优资助启动基金[(2009)416号文件] 云南省科技厅应用基础研究面上项目科研基金(编号:2007C0026R)
关键词 乳腺癌 组蛋白去乙酰化酶抑制剂 辛二酰苯胺异羟肟酸 动物模型 Breast neoplasm Histone deacetylase inhibitor N-Hydroxy-N-phenyloctanediamide Animal model
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  • 1Flis S,Gnyszka A,Splawinski J.HDAC inhibitors,MS275 and SBHA,enhances cytotoxicity induced by oxaliplatin in the colorectal cancer cell lines[J].Biochem Biophys Res Commun,2009,387(2):336.
  • 2Mariadason JM.HDACs and HDAC inhibitors in colon cancer[J].Epigenetics,2008,3(1):28.
  • 3Weichert W,Roske A,Niesporek S,et al.Class I histone d-eacetylase expression has independent prognostic impact in human cancer:Specific role of class I histone deacetylases in vitro and in vivo[J].Clin Cancer Res,2008,14(6):1669.
  • 4Bracker TU,Sommer A,Fichtner I.Efficacy of MS-275,a selective inhibitor of class I histone deacetylases,in human colon cancer models[J].Int J Oncol,2009,35(4):909.
  • 5Zhang F,Zhang T,Teng ZH.Sensitization to gamma-irradiation-induced cell cycle arrest and apoptosis by the histone deacetylase inhibitor trichostatin A in non-small cell lung cancer (NSCLC) cells[J].Cancer Biol Ther,2009,8(9):823.
  • 6Nishioka C,Ikezoe T,Yang J,et al.MS-275,a novel histone deacetylase inhibitor with selectivity against HDAC1,induces degradation of FLT3 via inhibition of chaperone function of heat shock protein 90 in AML cells[J].Leuk Res,2008,32(9):1382.
  • 7Kang MR,Kang JS,Han SB,et al.A novel delta-lactam-based histone deacetylase inhibitor,KBH-A42,induces cell cycle arrest and apoptosis in colon cancer cells[J].Biochem Pharmacol,2009,78(5):486.
  • 8Sun C,Zhou J.Trichostatin A improves insulin stimulated glucose utilization and insulin signaling transduction through the repression of HDAC2[J].Biochem Pharmacol,2008,76(1):120.
  • 9Gahr S,Peter G,Wissniowski TT.The histone-deacetylase inhibitor MS-275 and the CDK-inhibitor CYC-202 promote anti-tumor effects in hepatoma cell lines[J].Oncol Rep,2008,20(5):1249.
  • 10Habold 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.

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  • 1RaymondADANIELS,HelenTURLEY,FionaCKIMBERLEY,XueSongLIU,JuthathipMONGKOLSAPAYA3,PaulCH'EN,XiaoNingXU,BoquanJIN,FrancescoPEZZELLA,GavinRSCREATON.Expression of TRAIL and TRAIL receptors in normal and malignant tissues[J].Cell Research,2005,15(6):430-438. 被引量:22
  • 2王颖,王生余,侯春梅,徐元基,杜芝燕,于晓妉.组蛋白去乙酰化酶抑制剂SAHA阻断MAPK信号通路并诱导HL-60细胞凋亡[J].中国实验血液学杂志,2007,15(2):267-271. 被引量:3
  • 3Kim DH, Kim M, Kwnn HJ. Histone Deacetylase in carcinogenesis and its inhibitors as anti-cancer agents [ J ]. J Biochem Mol Biol, 2003,36( 1 ) :110-119.
  • 4Mann BS,Johnson JR, Cohen MH, et al. FDA approval summary: vorinostat for treatment of advanced primary cutaneous T-cell lym- phoma [ J ]. Oncologist, 2007,2 ( 10 ) : 1247-1252.
  • 5Yin D, Ong JM, Hu J, et al. Suberoylanilide hydroxamic acid, a his- tone deaeetylase inhibitor:effects on gene expression and growth of glioma cells in vitro and in vivo[ J]. Clin Cancer Res,2007,13 (3) :1045-1052.
  • 6Jin JS, Tsao TY, Sun PC, et al. SAHA inhibits the growth of colon tumors by decreasing histone deacetylase and the expression of eye- lin D1 and survivin[ J]. Patho] Oneol Res ,2012,18 ( 3 ) :713-720.
  • 7Munster PN, Troso-Sandoval T, Rosen N, et al. The histone deacetylase inhibitor suberoylanilide hydroxamic acid induces dif- ferentiation of human breast cancer cells[ J]. Cancer Res,2001,61 ( 23 ) : 8492-8497.
  • 8Kwon A, Park HJ, Back K, et al. Suberoylanilide hydroxamic acid enhances odontoblast differentiation [ J ]. J Dent Res,2012,91 ( 5 ) : 506-512.
  • 9Gillenwater AM, Zhong M, Lotan R. Histone deacetylase inhibitor suberoylanilide hydroxamic acid induces apoptosis through both mi- tochondrial and Fas( CD95 ) Signaling in head and neck squamous carcinoma cells[J]. Mol Cancer Ther,2007,6( 11 ) :2967-2975.
  • 10Ruefli AA, Bernhard D,Tainton KM,et al. Suberoylanilide hydrox- amic acid(SAHA) overcomes muhidrug resistance and induces cell death in P-glycoprotein-expressing cells[ J]. Int J Cancer,2002,99 ( 2 ) :292-298.

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