ATM相关信号通路在鼻咽癌中的作用研究进展
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Research progress on the role of ATM-related signaling pathway in nasopharyngeal carcinoma
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    摘要:

    鼻咽癌是一种与EB病毒感染密切相关的头颈部恶性肿瘤,其发病机制尚未完全阐明。放射治疗是鼻咽癌最主要的治疗手段,而放疗抵抗则容易使肿瘤复发或转移并最终导致放疗失败。共济失调毛细血管扩张突变(ATM)基因主要在DNA双键断裂时被激活,可参与调控DNA损伤修复、细胞周期阻滞和凋亡等过程。研究表明,ATM在鼻咽癌发生发展的不同阶段以及治疗干预的过程中发挥不同的作用,并在鼻咽癌的放疗抵抗中扮演着重要的角色。近年来,通过抑制ATM活性来降低放疗抵抗已成为学者们研究的热点。本文就ATM相关信号通路在鼻咽癌中的作用研究进展进行简要综述,为鼻咽癌的治疗提供参考。

    Abstract:

    Nasopharyngeal carcinoma(NPC) is a kind of head and neck malignant tumor closely related to Epstein-Barr virus infection, and its pathogenesis has not been fully elucidated. Radiotherapy is the main treatment for nasopharyngeal carcinoma, while radio-resistance is easy to cause tumor recurrence or metastasis and ultimately lead to radiotherapy failure. Ataxia-telangiectasia mutated (ATM) gene is mainly activated when DNA double-strand breaks. ATM can participate in the regulation of DNA damage repair, cell cycle arrest and apoptosis. Studies have shown that ATM plays different roles in different stages of NPC development and in the process of therapeutic intervention. ATM also plays an important role in the radio-resistance of NPC. In recent years, a method for reducing the radio-resistance of tumors by inhibiting ATM activity has become a research hotspot. This paper briefly reviews the role and research progress of ATM-related signaling pathways in NPC, which will provide reference for the treatment of NPC.

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    参考文献
    [1] Wong KCW, Hui EP, Lo KW, et al. Nasopharyngeal carcinoma:an evolving paradigm[J]. Nat Rev Clin Oncol, 2021, 18(11):679-695.
    [2] Perri F, Della Vittoria Scarpati G, Caponigro F, et al. Management of recurrent nasopharyngeal carcinoma:current perspectives[J]. Onco Targets Ther, 2019, 12:1583-1591.
    [3] Phan LM, Rezaeian AH. ATM:main features, signaling pathways, and its diverse roles in DNA damage response, tumor suppression, and cancer development[J]. Genes (Basel), 2021, 12(6):845.
    [4] Nie X, Guo E, Wu C, et al. SALL4 induces radioresistance in nasopharyngeal carcinoma via the ATM/Chk2/p53 pathway[J]. Cancer Med, 2019, 8(4):1779-1792.
    [5] Amirifar P, Ranjouri MR, Yazdani R, et al. Ataxia-telangiectasia:A review of clinical features and molecular pathology[J]. Pediatr Allergy Immunol, 2019, 30(3):277-288.
    [6] Lee JH, Paull TT. Cellular functions of the protein kinase ATM and their relevance to human disease[J]. Nat Rev Mol Cell Biol, 2021, 22(12):796-814.
    [7] Savitsky K, Bar-shira A, Gilad S, et al. A single ataxia telangiectasia gene with a product similar to PI-3 kinase[J]. Science, 1995, 268(5218):1749-1753.
    [8] Putti S, Giovinazzo A, Merolle M, et al. ATM Kinase Dead:From ataxia telangiectasia syndrome to cancer[J]. Cancers (Basel), 2021, 13(21):5498.
    [9] Ray U, Raghavan SC. Understanding the DNA double-strand break repair and its therapeutic implications[J]. DNA Repair (Amst), 2021, 106:103177.
    [10] Baretić D, Pollard HK, Fisher DI, et al. Structures of closed and open conformations of dimeric human ATM[J]. Sci Adv, 2017, 3(5):e1700933.
    [11] Qiu S, Huang J. MRN complex is an essential effector of DNA damage repair[J]. J Zhejiang Univ Sci B, 2021, 22(1):31-37.
    [12] Wang Q, Goldstein M, Alexander P, et al. Rad17 recruits the MRE11-RAD50-NBS1 complex to regulate the cellular response to DNA double-strand breaks[J]. EMBO J, 2014, 33(8):862-877.
    [13] Lee JH, Paull TT. ATM activation by DNA double-strand breaks through the Mre11-Rad50-Nbs1 complex[J]. Science, 2005, 308(5721):551-554.
    [14] Ueno S, Sudo T, Hirasawa A. ATM:Functions of ATM kinase and its relevance to hereditary tumors[J]. Int J Mol Sci, 2022, 23(1):523.
    [15] Olcina MM, Foskolou IP, Anbalagan S, et al. Replication stress and chromatin context link ATM activation to a role in DNA replication[J]. Mol Cell, 2013, 52(5):758-766.
    [16] Guo Z, Kozlov S, Lavin MF, et al. ATM activation by oxidative stress[J]. Science, 2010, 330(6003):517-521.
    [17] Shibata A, Jeggo PA. ATM's role in the repair of DNA double-strand breaks[J]. Genes (Basel), 2021, 12(9):1370.
    [18] Garcia-santisteban I, Llopis A, Krenning L, et al. Sustained CHK2 activity, but not ATM activity, is critical to maintain a G1 arrest after DNA damage in untransformed cells[J]. BMC Biol, 2021, 19(1):35.
    [19] Liu K, Zheng M, Lu R, et al. The role of CDC25C in cell cycle regulation and clinical cancer therapy:a systematic review[J]. Cancer Cell Int, 2020, 20:213.
    [20] Cheng Q, Chen J. Mechanism of p53 stabilization by ATM after DNA damage[J]. Cell Cycle, 2010, 9(3):472-478.
    [21] Magnussen HM, Ahmed SF, Sibbet GJ, et al. Structural basis for DNA damage-induced phosphoregulation of MDM2 RING domain[J]. Nat Commun, 2020, 11(1):2094.
    [22] Georgakilas AG, Martin OA, Bonner WM. p21:A two-faced genome guardian[J]. Trends Mol Med, 2017, 23(4):310-319.
    [23] Wang H, Shi LZ, Wong CC, et al. The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair[J]. PLoS Genet, 2013, 9(2):e1003277.
    [24] Han J, Wan L, Jiang G, et al. ATM controls the extent of DNA end resection by eliciting sequential posttranslational modifications of CtIP[J]. Proc Natl Acad Sci U S A, 2021, 118(12):e2022600118.
    [25] Mirman Z, De Lange T. 53BP1:a DSB escort[J]. Genes Dev, 2020, 34(1-2):7-23.
    [26] Hau PM, Deng W, Jia L, et al. Role of ATM in the formation of the replication compartment during lytic replication of Epstein-Barr virus in nasopharyngeal epithelial cells[J]. J Virol, 2015, 89(1):652-668.
    [27] Bose S, Yap LF, Fung M, et al. The ATM tumour suppressor gene is down-regulated in EBV-associated nasopharyngeal carcinoma[J]. J Pathol, 2009, 217(3):345-352.
    [28] Ko JJ, Klimowicz AC, Jagdis A, et al. ATM, THMS, and RRM1 protein expression in nasopharyngeal carcinomas treated with curative intent[J]. Head Neck, 2016, 38(Suppl 1):E384-391.
    [29] Frappier L. Epstein-Barr virus:Current questions and challenges[J]. Tumour Virus Res, 2021, 12:200218.
    [30] Lung RW, Hau PM, Yu KH, et al. EBV-encoded miRNAs target ATM-mediated response in nasopharyngeal carcinoma[J]. J Pathol, 2018, 244(4):394-407.
    [31] Kudoh A, Fujita M, Zhang L, et al. Epstein-Barr virus lytic replication elicits ATM checkpoint signal transduction while providing an S-phase-like cellular environment[J]. J Biol Chem, 2005, 280(9):8156-8163.
    [32] Hu J, Li H, Luo X, et al. The role of oxidative stress in EBV lytic reactivation, radioresistance and the potential preventive and therapeutic implications[J]. Int J Cancer, 2017, 141(9):1722-1729.
    [33] Hau PM, Tsao SW. Epstein-Barr Virus hijacks DNA damage response transducers to orchestrate its life cycle[J]. Viruses, 2017, 9(11):341.
    [34] Guan S, Wei J, Huang L, et al. Chemotherapy and chemo-resistance in nasopharyngeal carcinoma[J]. Eur J Med Chem, 2020, 207:112758.
    [35] Li MY, Liu JQ, Chen DP, et al. Radiotherapy induces cell cycle arrest and cell apoptosis in nasopharyngeal carcinoma via the ATM and Smad pathways[J]. Cancer Biol Ther, 2017, 18(9):681-693.
    [36] Vogin G, Bastogne T, Bodgi L, et al. The phosphorylated ATM immunofluorescence assay:A high-performance radiosensitivity assay to predict postradiation therapy overreactions[J]. Int J Radiat Oncol Biol Phys, 2018, 101(3):690-693.
    [37] Wang Q, Chen Y, Chang H, et al. The role and mechanism of ATM-mediated autophagy in the transition from hyper-radiosensitivity to induced radioresistance in lung cancer under low-dose radiation[J]. Front Cell Dev Biol, 2021, 9:650819.
    [38] Zhou X, Zheng J, Tang Y, et al. EBV encoded miRNA BART8-3p promotes radioresistance in nasopharyngeal carcinoma by regulating ATM/ATR signaling pathway[J]. Biosci Rep, 2019, 39(9):BSR20190415.
    [39] Ma X, Yang L, Xiao L, et al. Down-regulation of EBV-LMP1 radio-sensitizes nasal pharyngeal carcinoma cells via NF-kappaB regulated ATM expression[J]. PLoS One, 2011, 6(11):e24647.
    [40] Zhang B, Cui B, Du J, et al. ATR activated by EB virus facilitates chemotherapy resistance to cisplatin or 5-fluorouracil in human nasopharyngeal carcinoma[J]. Cancer Manag Res, 2019, 11:573-585.
    [41] Poon RY. DNA damage checkpoints in nasopharyngeal carcinoma[J]. Oral Oncol, 2014, 50(5):339-344.
    [42] Huang RX, Zhou PK. DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer[J]. Signal Transduct Target Ther, 2020, 5(1):60.
    [43] Sadoughi F, Mirsafaei L, Dana PM, et al. The role of DNA damage response in chemo- and radio-resistance of cancer cells:Can DDR inhibitors sole the problem?[J]. DNA Repair (Amst), 2021, 101:103074.
    [44] Jin MH, Oh DY. ATM in DNA repair in cancer[J]. Pharmacol Ther, 2019, 203:107391.
    [45] Wang M, Liu G, Shan GP, et al. In vivo and in vitro effects of ATM/ATR signaling pathway on proliferation, apoptosis, and radiosensitivity of nasopharyngeal carcinoma cells[J]. Cancer Biother Radiopharm, 2017, 32(6):193-203.
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周威邦,杨佩宣,程小凌,张小兵. ATM相关信号通路在鼻咽癌中的作用研究进展[J].中国耳鼻咽喉颅底外科杂志,2023,29(4):96-101

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  • 收稿日期:2022-07-04
  • 在线发布日期: 2023-08-31
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