放射诱导旁观者效应的研究进展
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  • 作者:龚玉华 ; 徐中叶
  • 关键词:旁观者效应 ; 放射治疗 ; 辐射效应
  • 中文刊名:YLZB
  • 英文刊名:Medical Equipment
  • 机构:江苏省无锡市人民医院;
  • 出版日期:2019-01-15
  • 出版单位:医疗装备
  • 年:2019
  • 期:v.32;No.374
  • 语种:中文;
  • 页:YLZB201901128
  • 页数:3
  • CN:01
  • ISSN:11-2217/R
  • 分类号:207-209
摘要
放射诱导的旁观者效应(RIBE)指未被直接辐射的细胞变现出与受照射细胞相类似的应答反应,这一现象的存在已经得到大量实验的证实。然而从发现该现象至今,其精确机制仍然不清楚。研究发现该现象的发生与多种机制相关,包括细胞缝隙连接(GJ)、可溶性因子的分泌、氧代谢等。现对放射诱导旁观者效应的研究方法和可能涉及的机制做一综述。
        
引文
[1]Hamada N,Maeda M,Otsuka K,et al.Signaling pathways underpinning the manifestations of ionizing radiation-induced bystander effects[J].Curr Mol Pharmacol,2010,14(2):79-95.
    [2]Nagasawa H,Little JB.Induction of sister chromatid exchanges by low doses ofα-particles[J].Cancer Res,1992,52(22):6394-6396.
    [3]Mothersill C,Lyng F,Seymour C,et al.Genetic factors influencing bystander signaling in murine bladder epitheliumafter low-dose irradiation in vivo[J].Radiat Res,2005,163(4):391-399.
    [4]Yang H,Asaad N,Held KD.Medium-mediated intercellular communication is involved in bystander responses of X-ray-irradiated normal human fibroblasts[J].Oncogene,2005,24(12):2096-2103.
    [5]郝希山,魏于全.肿瘤学[M].北京:人民卫生出版社,2010:298.
    [6]Shao C,Folkard M,Michael BD,et al.Bystander signaling between glioma cells and fibroblasts targeted with counted particles[J].Int JCancer,2005,116(1):45-51.
    [7]Shao C,Folkard M,Michael BD,et al.Targeted cytoplasmic irradiation induces bystander responses[J].Proc Natl Acad Sci U S A,2004,101(37):13495-13500.
    [8]Burdak-Rothkamm S,Short SC,Folkard M,et al.ATR-dependent radiation-induced gamma H2AX foci in bystander primary human astrocytes and glioma cells[J].Oncogene,2007,26(7):993-1002.
    [9]Hamada N,Matsumoto H,Hara T,et al.Intercellular and intracellular signaling pathways mediating ionizing radiationinduced bystander effects[J].J Radiat Res,2007,48(2):87-95.
    [10]Burdak-Rothkamm S,Prise KM.New molecular targets in radiotherapy:DNA damage signalling and repair in targeted and non-targeted cells[J].Eur J Pharmacol,2009,625(1-3):151-155.
    [11]Kashino G,Suzuki K,Matsuda N,et al.Radiation induced bystander signals are independent of DNA damage and DNA repair capacity of the irradiated cells[J].Mutat Res,2007,619(1-2):134-138.
    [12]Kashino G,Prise KM,Schettino G,et al.Evidence for induction of DNA double strand breaks in the bystander response totargeted soft X-rays in CHO cells[J].Mutat Res,2004,556(1-2):209-215.
    [13]Shao C,Lyng FM,Folkard M,et al.Calcium fluxes modulate the radiation-induced bystander responses in targeted glioma and fibroblast cells[J].Radiat Res,2006,166(3):479-487.
    [14]王中堂,唐宪民.放射诱导旁观者效应的研究进展[J].国际肿瘤学杂志,2006,33(5):344-347.
    [15]Shao C,Prise KM,Folkard M.Signaling factors for irradiated glioma cells induced bystander responses in fibroblasts[J].Mutat Res,2008,638(1-2):139-145.
    [16]Chen S,Zhao Y,Zhao G,et al.Up-regulation of ROS by mitochondria-dependent bystander signaling contributes to genotoxicity of bystander effects[J].Mutat Res,2009,666(1-2):68-73.
    [17]Zhou H,Ivanov VN,Lien YC,et al.Mitochondrial function and nuclear factor-kappaB-mediated signaling in radiation-induced bystander effects[J].Cancer Res,2008,68(7):2233-2240.
    [18]Chen S,Zhao Y,Han W,et al.Mitochondria-dependent signalling pathway are involved in the early process of radiation-induced bystander effects[J].Br J Cancer,2008,98(11):1839-1844.
    [19]Pasi F,Facoetti A,Nano R.IL-8 and IL-6 bystander signalling in human glioblastoma cells exposed to gamma radiation[J].Anticancer Res,2010,30(7):2769-2772.
    [20]Coates PJ,Rundle JK,Lorimore SA,et al.Indirect macrophage responses to ionizing radiation:implications for genotypedependent bystander signaling[J].Cancer Res,2008,68(2):450-456.
    [21]凌诒萍.细胞生物学[M].北京:人民卫生出版社,2006:72-74.
    [22]Shao C,Furusawa Y,Aoki M,et al.Role of gap junctional intercellular communication in radiation-induced bystander effects in human fibroblasts[J].Radiat Res,2003,160(3):318-323.

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