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DNA-PKcs影响肝癌耐药细胞BEL7402/5-FU耐药性的机制 被引量：2

The effect of DNA-PKcs gene silence on the expression of Artemis and P-Artemis in liver cancer BEL7402 /5-FU cells
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摘要 目的利用RNA干扰技术探讨DNA-PKcs基因沉默影响肝癌细胞BEl7402/5-FU耐药性的机制。方法将靶向DNA-PKcs的干扰质粒shDNA-PKcs转染肝癌耐药细胞BEL7402/5-FU,利用实时荧光定量PCR及Western blot法检测转染干扰质粒后DNA-PKcs基因的沉默效率;Western blot检测Artemis、磷酸化Artemis蛋白水平的表达。结果实时荧光定量PCR及Western blot检测结果显示转染shDNA-PKcs后,DNA-PKcs mRNA及蛋白水平表达均下调(P<0.05);Western blot检测结果显示shDNA-PKcs转染组Artemis蛋白表达水平与对照组相比均有所降低(P<0.05),磷酸化Artemis蛋白表达水平在转染前后无明显变化(P>0.05)。结论 ShDNA-PKs干扰质粒能抑制Bel-7402/5FU细胞中DNAPKcs、Artemis蛋白的表达、但对P-Artemis的表达无影响。 Objective To observe the effect of DNA-PKcs gene silencing on the mechanism of drug resistance in Bel7402 /5-FU by RNA interference technology.Methods Targeted DNA-PKcs interference plasmid was transfected into liver cancer cell BEL7402 /5-FU.DNA-PKcs silencing efficiency was detected by Real-time PCR and Western blot.The expression of Artemis and P-Artemis by Western blot.Results Real-time PCR and Western blot assay indicated that the mRNA and protein levels of DNA-PKcs expression were downregulated after transfection of shDNA-PKcs（ P〈0.05）.Western blot analysis showed that the expression of Artemis was decreased on protein levels compared with the control group（ P〈0.05）;P-Artemis protein expression level was not changed before and after transfection compared with the control group（ P〉0.05）.Conclusion The shDNA-PKcs reduces DNA-PKcs and Artemis expression in BEL7402 /5-FU cells,but had no effect on the expression of P-Artemis.
作者 李长福 梁大敏 束波 杨加伟 生欣 范芳
机构地区 遵义医学院生物化学教研室
出处 《遵义医学院学报》 2014年第5期517-519,528,共4页 Journal of Zunyi Medical University
基金 贵州省社发攻关项目(NO:[2009]3066)
关键词 DNA依赖性蛋白激酶催化亚基 多药耐药 ARTEMIS DNA-PKcs multidrug resistance Artemis
分类号 R735.7 [医药卫生—肿瘤]
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参考文献14

  • 1Lord C J, Ashworth A. The DNA damage response and canc- er therapy[J]. Nature, 2012, 481(7381) : 287 -294.
  • 2Curtin N J. DNA repair dysregulation from cancer driver to therapeutic target [ J ]. Nat Rev Cancer, 2012, 12 (12) : 801 -817.
  • 3Hsu F M, Zhang S, Chen B P. Role of DNA - dependent protein kinase catalytic subunit in cancer development and treatment[J]. Transl Cancer Res, 2012, 1 ( 1 ) : 22 -34.
  • 4Lee K J, Lin Y F, Chou H Y, et al. Involvement of DNA -dependent protein kinase in normal cellcycleprogression through mitosis[J]. J Biol Chem,2011,286(14) : 12796 - 12802.
  • 5梁大敏,束波,杨加伟,生欣,范芳.shRNA沉默DNA-PKcs表达对肝癌耐药细胞BEL7402/5-FU耐药性的影响[J].遵义医学院学报,2014,37(3):304-307. 被引量：7
  • 6Uematsu N, Weterings E, Yano K, et al. Autophosphory- lation of DNA - PKCS regulates its dynamics at DNA double - strand breaks [ J ]. J Cell Biol, 2007,177 ( 2 ) : 219 -229.
  • 7Nishida Y, Mizutani N, Inoue M, et al. Phosphorylated Spl is the regulator of DNA - PKcs and DNA ligase IV transcription of daunorubicin - resistant leukemia cell lines [J]. Biochim Biophys Acta,2014,1839(4) : 265 -274.
  • 8Evert M, Frau M, Tomasi M L, et al. Deregulation of DNA- dependent protein kinase catalytic subunit contrib- utes to human hepatocarcino genesis development and has a putative prognostic value [ J ] Br J Cancer, 2013, 109 (10) :2654 -2664.
  • 9Cornell L,Munck J, Curtin N, et al. PTU - 042 DNA - PKor ATM inhibition inhibits non - homologous end join- ing and enhances ehemo - and radio sensitivity in hepato- cellular eancer cell lines [ J ]. Gut ,2012,61 : A201.
  • 10Lundholm L, Hgtg P, Zong D, et al. Resistance to DNA -damaging treatment in non- small cell lung cancertumor - initiating cells involves reduced DNA - PK/ATM activation and diminished cell cycle arrest [ J ]. Cell Death Dis, 2013, 4: e478.

二级参考文献12

  • 1Lee K J,Lin Y F,Chou H Y,et al.Involvement of DNA-dependent protein kinase in normal cellcycleprogression through mitosis[J].J Biol Chem,2011,286(14):12796-12802.
  • 2Hsu F M,Zhang S,Chen B P.Role of DNA-dependent protein kinasecatalytic subunit in cancerdevelopment and treatment[J].Transl Cancer Res,2012,1 (1):22-34.
  • 3Seo S B,Hur J G,Kim M J,et al.TRAIL sensitize MDR cells to MDR-related drugs by down-regulation of P-glycoprotein through inhibition of DNA-PKcs/Akt/GSK-3beta pathway and activation of caspases[J].Mol Cancer,2010,28 (9):199.
  • 4Lee P C,Lee H J,Kakadiya R,et al.Multidrug-resistant cells over expressing P-glycoprotein are susceptible to DNA crosslinking agents due to attenuated Src/nuclear EGFR cascade-activated DNA repair activity[J].Oncogene,2013,32(9):1144-1154.
  • 5Bouwman P,Jonkers J.The effects of deregulated DNA damage signalling on cancer chemotherapy response and resistance[J].Nat Rev Cancer,2012,12 (9):587-598.
  • 6Curtin N J.DNA repair dysregulation from cancer driver to therapeutic target[J].Nat Rev Cancer,2012,12(12):801-817.
  • 7Rothkamm K,Krüger I,Thompson L H,et al.Pathways of DNA double-strand break repair during the mammalian cell cycle[J].Mol Cell Biol,2003,23(16):5706-5715.
  • 8Evert M,Frau M,Tomasi M L,et al.Deregulation of DNA-dependent protein kinase catalytic subunit contributes to human hepatocarcino genesis development and has a putative prognostic value[J].Br J Cancer,2013,109(10):2654-2664.
  • 9Cornell L,Munck J,Curtin N,et al.PTU-0420 DNA-PKor ATM inhibition inhibits non-homologous end joining and enhances chemo-and radio sensitivity in hepatocellular cancer cell lines[J].Gut,2012,61:A201.
  • 10Stderlund Leifler K,Queseth S,Fornander T,et al.Low expression of Ku70/80,but high expression of DNA-PKcs,predict good response to radiotherapy in early breast cancer[J].Int J Oncol,2010,37 (6):1547-1554.

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遵义医学院学报
2014年 第5期

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