期刊文献+

性激素抑制活性氧诱导肝癌细胞增殖的实验研究 被引量:2

Cell proliferation induced by estrogen and androgen inhibiting reactive oxygen species in liver cancer
原文传递
导出
摘要 目的:探讨性激素和活性氧协同作用对肝癌细胞增殖的影响。方法:采用MTT法观察性激素(雌二醇或睾酮)和H2O2单独处理或同时处理表达性激素受体的Hepa1-6细胞的增殖率。结果:浓度<10μmol/L的雌二醇或睾酮对细胞的增殖无显著影响。H2O2浓度为1~15μmol/L时,促进细胞增殖。>100μmol/L则抑制细胞的增殖甚至诱导细胞的凋亡和坏死。雌激素或雄激素与15μmol/LH2O2联合使用时,细胞增殖消失;与200μmol/LH2O2联合使用时,增强了H2O2对细胞的毒性作用。性激素可抑制低浓度H2O2诱导的细胞增殖效应并可加强中等浓度H2O2的细胞损伤作用。结论:性激素与活性氧的相互作用抑制了细胞的增殖,为进一步探讨性激素与活性氧的相互作用关系提供了实验依据,为性激素依赖或相关性肿瘤的治疗提供了新的思路。 OBJECTIVE:To explore the relationship between reactive oxygen species(ROS)and sex hormones on liver cancer cell proliferation.METHODS:The hepa1-6 cells were treated by H2O2 and sex hormones(testosterone and estradiol)separately or simultaneously,and then the cell proliferations were investigated by the MTT method.RESULTS:The sex hormones did not significantly influence the cell proliferation up to the concentration of 10 μmol/L.For H2O2,the cell proliferation significantly improved at the low concentration(1-15 μmol/L).However,the cell proliferation was significantly inhibited or the cells were induced to death at the high concentration(〉100 μmol/L).Interestingly,when the cells were treated simultaneously with sex hormones and H2O2,the promotion function of low concentration of H2O2(15 μmol/L)was impaired and the inhibitory function of high concentration of H2O2(20 μmol/L)was promoted by sex hormones.CONCLUSION:Sex hormones impair the promotion function of low concentration of H2O2 to the cell proliferation and promote the inhibition function of middle concentration of H2O2 to the cell proliferation.
出处 《中华肿瘤防治杂志》 CAS 2010年第5期326-329,共4页 Chinese Journal of Cancer Prevention and Treatment
基金 国家自然科学基金(30872950-C171002) 辽宁省教育厅基金(2008031) 教育部留学回国基金
关键词 雌激素 雄激素 活性氧 细胞增殖 肝肿瘤 estrogen androgen reactive oxygen species cell proliferation liver neoplasms
  • 相关文献

参考文献3

二级参考文献26

  • 1Ryung-Ah Lee,Hyun-Ah Kim,Bo-Young Kang,Kwang-Ho Kim.Hemoglobin induces colon cancer cell proliferation by release of reactive oxygen species[J].World Journal of Gastroenterology,2006,12(35):5644-5650. 被引量:1
  • 2Schafer D F,Sorrell M F.Hepatocellular carcinoma[J].Lancet,1999,353(9160):1253-1257.
  • 3Nagasue N,Ito A,Yukaya H,et al.Estrogen receptors in hepatocellular carcinoma[J].Cancer,1986,57(1):87-91.
  • 4Doerfler W.On the biological significance of DNA methylation[J].Biochemistry (Moscow),2005,70(5):505-524.
  • 5Edmondson H A,Steiner P E.Primary carcinoma of the liver:a study of 100 cases among 48,900 necropsies[J].Cancer,1954,7(3):462-503.
  • 6Bender C M,Pao M M,Jones P A.Inhibition of DNA methylation by 5-Aza-2'-deoxycytidine suppresses the growth of human tumor cell lines[J].Cancer Res,1998,58(1):95-101.
  • 7Herman J G,Graff J R,Myohanen S,et al.Methylation-specific PCR:a novel PCR assay formethylation status of CpG islands[J].Proc Natl Acad Sci USA,1996,93(18):9821-9826.
  • 8Lapidus R G,Nass S J,Butash K A,et al.Mapping of ER gene CpG island methylation-specific polymerase chain reaction[J].Cancer Res,1998,58 (12):2515-2519.
  • 9Takano N,Iizuka N,Hazama S,et al.Expression of estrogen receptor-alpha and -beta mRNAs in human gastric cancer[J].Cancer Lett,2002,176(2):129-135.
  • 10Bosch F X,Ribes J,Borras J.Epidemiology of primary liver cancer[J].Semin Liver Dis,1999,19(3):271-285.

共引文献25

同被引文献40

  • 1Glimcher LH. XBP1 : the last two decades[-J. Ann Rheum Dis, 2010,69(Suppl 1):67 71.
  • 2Koong AC,Chauhan V,Romero Ramirez L. Targeting XBP-1 as a novel anti cancer strategyJ. Cancer Biol 8,- Ther, 2006,5 (7) :756-759.
  • 3Hetz C, Martinon F, Rodriguez D, et al. The unfolded protein re sponseintegrating stress signals through the stress sensor IRElaJ. Physiol Rev,2011,91(4):1219-1243.
  • 4Glimcher LH, Lee AH. From sugar to fat how the transcription factor XBP1 regulates hepatic lipogenesisJ. Ann N Y Acad Sci,2009,1173 Suppl l:E2-E9.
  • 5Van Schadewiik A,Van't Wout EF,Stolk J,et al. A quantitative method for detection of spliced X box binding protein-1 (XBP1) mRNA as a measure of endoplasmic reticulum (ER)stress. Cell Stress Chaperones,2012,17(2) =275-279.
  • 6MinvilleWalz M, Pierre AS, Pichon L, et al. Inhibition of stearoyl- CoA desaturase 1 expression induces CHOP-dependent cell death in human cancer cells. Plo, 2010,5 (12) = e14363.
  • 7Run D, Walter P. Signal integration in the endoplasmic reticulum unfolded protein response. Nat Rev Mol Cell Biol, 2007,8 (7) :519-529.
  • 8Lee AH,Iwakoshi NN,Glimcher LH. XBP-1 regulates a subset of en- doplasmic reticulum resident chaperone genes in the unfolded protein reslmnse. Molecular Cdlular, 2003,23 ( 21) = 7448-7459.
  • 9Shaffer AL,Shapiro-Shelef M,Iwakoshi NN',et al. XBP1 ,down- stream of Bbmp-1, expands the secretory apparatus and other or- ganelles,and increases protein synthesis in plasma cell differenti- ation 1- Immunity, 2004,21 ( 1 ) : 81-93.
  • 10Sriburi R, Bommiasamy H,Buldak GL, et al. Coordinate regula tion of phospholipid biosynthesis and secretory pathway gene ex- pression in XBP 1 (S)-induced endoplasmic reticulum biogenesis[J]. J BiolChem,2007,282(10):7024-7034.

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部