脆性组氨酸三联体与细胞信号转导研究进展

杨剑 韩玲

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脆性组氨酸三联体与细胞信号转导研究进展

    通讯作者: 韩玲, linghan8888@yahoo.com.cn
  • 中图分类号: Q344.13

Progress on fragile histidine triad and cell signal transduction

    Corresponding author: HAN Ling, linghan8888@yahoo.com.cn
  • CLC number: Q344.13

  • 摘要: 脆性组氨酸三联体(FHIT)基因是一种抑癌基因,其与许多肿瘤的发生有密切的关系.近几年有关FHIT基因的研究,侧重于辐射后FHIT及其上下游调控基因之间的关系和作用方式,包括ATR/CHK1、bcl-2基因、caspase家族、环孢霉素A和核因子-κB之间的作用.
  • [1] Ohta M,Inoue H,Cotticelli MG,et al,Hie FHIT gene,spanning the chromosome 3pl4.2 fragile site and renal carcinoma-associated t(3;8) breakpoint,is abnormal in digestive tract cancer.Cell,1996,84(4):587-597.
    [2] Paulovich AG,Hartwell LH.A checkpoint regulates the rate of progression through S phase in S.cerivisiae in response to DNA damage.Cell,1995,75 (4): 841-847.
    [3] Abraham RT.Cell cycle checkpoint signaling through the ATM and ATR kinases.Genes Dev,2001,15(17):2177-2196.
    [4] Bakkenist CJ,Kastan MB.Initiating cellular stress responses.Cell,2004,118(1):9-17.
    [5] Shiloh Y.ATM and ATR:Networking cellular responses to DNA damage.Cuit Opin Genet Dev,2001,11(1):71-77.
    [6] Sancar A,Lindsey-Boltz LA,Unsal-Kacmaz K,et al.Molecular mechanisms of mammalian DNA repair and the DNA damage checkpoints.Annu Rev Biochem,2004,73:39-85.
    [7] Cliby WA,Roberts CJ,Cimprich KA,et al.Overexpression of a kinase-inactive ATR protein causes sensitivity to DNA-damaging agents and defects in cell cycle checkpoints.EMBO J,1998,17(1):159-169.
    [8] Hu B, Han SY,Wang X,et al.Involvement of the Fhit gene in the ionizing radiation-activated ATR/CHK1 pathway.J Cell Physiol,2005,202(2):518-523.
    [9] Hu B,Wang H,Wang X,et al.Fhit and CHK1 have opposing effects on homologous recombination repair.Cancer Res,2005,65 (19):8613-8616.
    [10] Ottey M,Han SY,Druck T,et al.Fhit deficient normal and cancer cells are mitomycin C and UVC resistant.Br J Cancer,2004,91(9):1669-1677.
    [11] Liang F,Han M,Romanienko PJ,et al.Homology-directed repair is a major double-strand break repair pathway in mammalian cells.Proc NatJ Acad Sci USA,1998,95(9):5172-5177.
    [12] Wang H,Wang X,Iliakis G,et al.Caffeine could not efficiently sensitize homologous recombination repair deficient cells to ionizing radiation-induced killing.Radiat Res,2003,159(3):420-425.
    [13] Wang X,Wang H,Iliakis G,et al.Caffeine-induced radios-ensitization is independent of nonhomologous end joining of DNA double strand breaks.Radiat Res,2003,159(3):426-432.
    [14] Kim CH,Yoo JS,Lee CT,et al.FHIT protein enhances paciitaxel-induced apoptosis in lung cancer cells.Int J Cancer,2006,118(7):1692-1698.
    [15] Vivanco I,Sawyers CL.The phosphatidylinositol 3-kinase AKT pathway in human cancer.Nat Rev Cancer,2002,2(7):489-501.
    [16] Semba S,Trapasso F,Fabbri M,et al.Fhit modulation of the Akt-survivin pathway in lung cancer cells:Fhit-tyrosine 114 (Y114) is essential.Oncogene,2006,25(20):2860-2872.
    [17] Ramesh R,Saeki T,Templeton NS,et al.Successful treatment of primary and disseminated human lung cancere by systemic delivery of tumor suppressor genes using an improved liposome vector.Mol Ther,2001,3 ⑶:337-350.
    [18] Sembas S,Huebner K.Protein expression profiling identifies cyclop-hilin A as a molecular target in Fhit-mediated tumor suppr-ession.Mol Cancer Res,2006,4(8):529-538.
    [19] Kahl CR,Means AR.Calcineurin regulates cyclin D1 accumulation in growth-stimulated fibroblasts.Mol Biol Cell,2004,15(4):1833-1842.
    [20] Nakagawa Y,Akao Y.Fhit protein inhibits cell growth by attenuating the signaling mediated by nuclear factor-κB in colon cancer celllines.Exp Cell Res,2006,312(13):2433-2442.
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  • 收稿日期:  2006-11-26

脆性组氨酸三联体与细胞信号转导研究进展

摘要: 脆性组氨酸三联体(FHIT)基因是一种抑癌基因,其与许多肿瘤的发生有密切的关系.近几年有关FHIT基因的研究,侧重于辐射后FHIT及其上下游调控基因之间的关系和作用方式,包括ATR/CHK1、bcl-2基因、caspase家族、环孢霉素A和核因子-κB之间的作用.

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