期刊文献+

线粒体DNA4977bp缺失检测肿瘤细胞辐射敏感性的初步研究 被引量:1

Predicting of radiosensitivity of human tumor cell lines in vitro by determining 4977bp deletion in mitochondrial DNA
暂未订购
导出
摘要 目的:探讨mtDNA4977bp缺失用于肿瘤细胞辐射敏感性检测的可行性。方法:分别采用MTT法和巢式PCR法测定人肿瘤细胞株—肝癌细胞(HepG2)、食管癌细胞(EC-9706)和乳腺癌细胞(MCF-7)不同剂量γ射线照射后的存活分数(SF)和mtDNA4977bp缺失率。结果:MTT法:2Gy、4Gy和8Gy照射后,HepG2和EC-9706的SF显著低于MCF-7,表明HepG2和EC-9706细胞具有更高的辐射敏感性,HepG2细胞照射后的SF略低于EC-9706细胞,但统计学差异不显著。PCR法:1Gy和4Gy照射后3种肿瘤细胞mtDNA4977bp缺失率无显著性差异。8Gy照射后HepG2和EC-9706 mtDNA4977bp缺失进一步增加,而MCF-7的缺失率下降,显著低于HepG2与EC-9706细胞的缺失率,但HepG2和EC-9706细胞的缺失率无统计学差异,提示HepG2和EC-9706细胞的辐射敏感性高于MCF-7细胞,这与MTT法测定结果相符。结论:测定mtDNA4977bp缺失作为快速、简便的检测方法,有望用于肿瘤细胞辐射敏感性预测。 Objective : To investigate the feasibility of determining radiosensitivity of tumor cell lines in vitro using the assay of mtDNA4977bp deletion . Methods: The surviving fraction(SF)and the ratio of mtDNA4977bp deletion were determined by MTT assay and nested PCR technique respectively after tumor cells of HepG2、 MCF-7 and EC-9706 were irradiated by various doses of 7-ray radiation from 0Gy to 8Gy. Results: MTT assay:The SF of HepG2 and EC-9706 after irradiated by 2Gy.4Gy and 8Gy radiation was lower significantly than that of MCF-7,which showed radiosensitivity of HepG2 and EC-9706 was higher than that of MCF-7. But there was no statistical difference of SF between HepG2 and EC-9706. PCR method :The differences on mtDNA 4977bp deletion in mitochondrial DNA between HepG2, EC-9706 and MCF-7 were not significant after 1Gy and 4Gy 7 radiation. The ratio of 4977bp deletion in mitochondrial DNA of HepG2 and EC-9706 increased while MCF-7 decreased after exposure to 8Gy radiation. The ratio of mtDNA 4977bp deletion of HepG2 and EC-9706 was higher significantly than that of MCF-7 after irradiated by 8Gy,which implied radiosensitivity of HepG2 and EC-9706 was higher than that of MCF-7,which is consistent with the result from MMT assay. But the ratio of mtDNA 4977bp deletion was not statistically different between HepG2 and EC-9706. Conclusion: The method of mtDNA4977bp deletion may be used as a marker to predict radiosensitivity of tumor cells.
出处 《陕西医学杂志》 CAS 北大核心 2008年第3期262-265,共4页 Shaanxi Medical Journal
基金 中国医学科学院放射医学研究所青年创新探索基金(S617) 天津市自然科学基金(07JCYBJC09200)
关键词 肿瘤 辐射性DNA 线粒体 细胞/辐射效应 比色法 聚合酶链反应 Neoplasms, radiationqnduced DNA, mitochondrial Cell/radiation effectsPolymerase chain reaction
  • 相关文献

参考文献8

二级参考文献33

  • 1李胜保,吴清明,王小虎,谢国建.环氧合酶-2抑制剂NS-398对食管癌细胞放射增敏作用及机制初探[J].中华放射肿瘤学杂志,2005,14(4):350-352. 被引量:3
  • 2[1]Arlett CF, Harcout SA. Survey of radiosensitivity in a variety of human cell strains [J ]. Cancer Res, 1980,40(3 ): 926 - 932.
  • 3[2]Lambin P,Coco Martin J,Legal JD,et al. Intrinsic radiosensitivity and chromosome aberration analysis using fluorescence in situ hybridization incells of two human tumor cell lines[J]. Radiat Res, 1994, 138( 1 Suppl): 40 - 43.
  • 4[3]Begg AC.Prediction ofrepopulation rates and radiosensitivity in human tumors[J]. Int J Radiat Biol, 1994,65( 1 ): 103 - 108.
  • 5[4]Evans JW, Liu XF, Kirchgessner CU, et al. Induction and repair of chromosome aberrations in scid cells measured by premature chromosome condensation [ J ]. Radiat Res, 1996,145 ( 1 ): 39 - 46.
  • 6[5]Matsumoto K,Ramsey MJ,Nelson DO,et al. Persistence of radiationinduced translocations in human peripheral blood determined by chromosome painting[J]. Radiat Res, 1998,149(6) :602 - 613.
  • 7[6]Nunez MI, Villalobas M, Olea N, et al. Radiation induced DNA double strand breaks rejoining in human tumor cells [J ]. Bri J Cancer, 1995, 71(2):311 -316.
  • 8[7]Sachs RK, Chen AM, Simpson PJ, et al. Clustering of radiation-produced breaks along chromosomes: modelling the effects on chromosome aderrations[J ] .Int J Radiat Biol, 1999,75(6) :657 - 672.
  • 9[8]Spruill MD, Nelson DO, Ramsey MJ, et al. Lifetime persistence and clonality of chromosome aberrations in the peripheral blood of mice acutely exposed to ionizing radiation[J ]. Radiat Res ,2000,153( 1 ): 110 - 121.
  • 10[9]Coco Martin JM, Begg AC. Detection of radiation-induced chromosomeaberrations using fluorescence in situ hybridization in drug-induced premature chromosome condensations of tumour cell lines with different radiosensitivities[J ]. Int J Radiat Biol, 1997,71 (3) :265 - 273.

共引文献41

同被引文献11

  • 1陈刚,杜卫东,曹慧敏.线粒体DNA突变与相关人类疾病[J].遗传,2007,29(11):1299-1308. 被引量:15
  • 2Osaki T, Tatemoto Y, Yoneda K, Yamamoto T. Tumorige- nicity of cell lines established from oralsquamous cell carcino- ma and its metastatic lymphnodes [J]. Eur J Cancer B Oral Oncol 1994, 30B : 296-301.
  • 3Modica-Napolitano JS, Singh KK. Mitochondrial dysfunc- tion in cancer [J]. Mitochondrion, 2004, 4(5-6) ; 755- 762.
  • 4Yakubovskaya E, Chen Z, Carrodeguas JA, et al. Functional human mitochondrial DNA polymerase gamma forms a het- erotrimer [J]. J Biol Chem, 2006, 281(1) :374-382.
  • 5Ropp PA, Copeland WC. Cloning and characterization ofthe- human mitochondrial DNA polymerase, DNA polymeraseg- amma [J]. Genomics, 1996, 36 :449-458.
  • 6Pinz KG, Bogenhagen DF. Efficient repair of ahasic sites inDNA bymitochondrialenzymes [J]. Mol Cell Biol, 1998, 18 : 1257-1265.
  • 7Popanda O, Seibold P, Nikolov I, et al. Germline variants of base excision repair igenes and breast cancer: A polymor- phism in DNA polymerase gamma modifies gene expression and breast cancer risk [J]. Int J Cancer, 2013, 132(1): 55 -62.
  • 8Correia RL, Oba-Shinjo SM, Uno M, et al. Mitochondrial DNA depletion and its correlation with TFAM, TFBIM, TFB2M and POLG in human diffusely infiltrating astrocyto- mas[J]. Mitochondrion, 2011, 11(1) : 48-53.
  • 9Qian W, Van Houten B. Alterations in bioenergetics due to changes in mitochondrial DNA copy number [J]. Methods, 2010, 51(4) : 452-457.
  • 10Singh KK, Ayyasamy V, Owens KM, et al. Mutations in mitochondrial DNA polymerase-gamma promote breast tu- morigenesis [J]. J Hum Genet, 2009, 54(9) : 516-524.

引证文献1

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