PI3K/Akt与胶质瘤辐射抗性

薛景; 刘芬菊

PI3K/Akt与胶质瘤辐射抗性

薛景 , 刘芬菊

文章导航 > 国际放射医学核医学杂志 > 2005, 29 > 1: (40-43)

引用本文:

Citation:

PI3K/Akt与胶质瘤辐射抗性

薛景,
刘芬菊

215006 苏州, 苏州大学放射医学与公共卫生学院
基金项目:
苏州大学医学发展基金重点项目资助(EE126031)
中图分类号: R730.55

PI3K/Akt and radioresistance of glioma

Radiation Medicine and Public Health School, Soochow University, Soochow 215006, China
CLC number: R730.55

摘要: 恶性脑胶质瘤的术后治疗是患者预后生存期延长的关键,如何提高肿瘤组织的辐射敏感性,增强正常组织的辐射抗性是当前肿瘤放射生物学及临床放疗研究的热点。研究资料表明,PI3K/Akt抗细胞凋亡通路的激活提高了部分细胞的辐射抗性,特别在表皮细胞受紫外线照射的研究中提示,辐射产生的活性氧可能是该通路激活的原因之一;电离辐射可能诱导相关的细胞因子通过激活PI3K/Akt通路介导胶质瘤细胞的辐射抗性;PI3K及其相关酶可能通过DNA修复途径发挥抗辐射作用。PI3K/Akt通路的研究可为放射治疗胶质瘤提供新型的增敏药。
- PI3K/Akt /
- 胶质瘤 /
- 辐射抗性
Abstract: s The post operation therapy on the malignant cerebral glioma is a key to the life extension of a patient. It is a hotspot in radiobiology of tumor and radiotherapy to study how to enhance the radiosensitivity of the tumor tissues and increase the radioresistance of the normal tissues. It was found that activation of PI3K/Akt pathway, an anti-apoptosis pathway, may result in enhancement of radioresistance of some cell lines. Particularly, in researches of ultraviolet (UV) radiation on epidermic cells. It was found that the reactive oxygen species(ROS) induced by UV may be one of the causes to activate the PI3K/Akt. Induction of relative cytokines by ionizing radiation may mediate radioresistance of glioma through PI3K/Akt. It was also found that PI3K and relative kinase may enhance radioresistance of cells through DNA repair. In a word, researches of PI3K/Akt pathway may provide some new radiosensitizers for radiotherapy of glioma.
- PI3K/Akt /
- glioma /
- radioresistance
本作品遵循Signature-Non-Commercial Use 4.0 International (CC BY-NC 4.0)协议

[1]	Castro MG, Cowen R, Wiiliamson IK, et al. Current and future strategies for the treatment of malignant brain tumors[J]. Pharmac Therapeutics, 2003, 98(1):71-108.
[2]	Yount GL, Afshar G, Ries S, et al. Transcriptional activation of TRADD mediates p53-independent radiation-induced apoptosis of glioma ceils[J]. Oncogene, 2001, 20(22):2826-2835.
[3]	翟中, 王喜忠, 丁明孝等.细胞生物学[M].北京:高等教育出版社,2000,464.
[4]	Tomita M, Suzuki N, Matsumoto Y, et al. Sensitization by wortmannin of heat- or X-ray induced cell death in cultured Chinese hamster V79 cells[J]. J Radiat Re, 2000, 41(2):93-102.
[5]	Cataldi A, Zauli G, Di Pietro R, et al. Involvement of the pathway phosphatidylinositol-3-kinase/AKT-1 in the establishment of the survival response to ionizing radiation[J]. Cell Signall, 2001, 13(5):369-375.
[6]	Tachiiri S, Sasai K, Oya N, et al. Enhanced cell killing by overexpression of dominant-negative phosphatidylinositol 3-kinase subunit, Deltap85, following genotoxic stresses[J]. Japan J Cancer Res, 2000, 91(12):1314-1318.
[7]	Edwards E, Geng L, Tan J, et al. Phosphatidylinositol 3-kinase/Akt signaling in the response of vascular endothelium to ionizing radiation[J]. Cancer Res, 2002, 62(16):4671-4677.
[8]	Wickremasinghe RG, Ganeshaguru K, Jones DT, et al. Autologous plasma activates Akt/protein kinase B and enhances basal survival and resistance to DNA damage-induced apoptesis in B-chronic lymphocytic leukaemia cells[J]. Br J Haematol, 2001, 114(3):608-615.
[9]	Jones DT, Ganeshaguru K, Anderson R J, et al. Albumin activates the AKT signaling pathway and protects B-chronic lymphocytic leukemia cells from chlormnbucil and radiation-induced apoptosis[J]. Blood, 2003, 101(8):3174-3180.
[10]	Cataldi A, Di Pietro R, Centurione L, et al. Engagement of PI-3-kinase mediated protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis[J]. Int J Oncol, 2003, 22(1):129-135.
[11]	Ibuki Y, Goto R. Suppression of apoptosis by UVB irradiation:survival signaling via PI3-kinase/Akt pathway[J]. Biochem & Biophys Res Commun, 2000, 279(3):872-878.
[12]	Wan YS, Wang ZQ, Shao Y, et al. Ultraviolet irradiation activates PI 3-kinase/AKT survival pathway via EGF receptors in human skin in vivo[J]. Int J Oncol, 2001, 18(3):461-466.
[13]	Zhang QS, Maddock DA, Chen JP, et al. Cytokine-indueed p38 activation feedback regulates the prolonged activation of AKT cell survival pathway initiated by reactive oxygen species in response to UV irradiation in human keratinocytes[J]. Int J Oneol,2001.19(5):1057-1061.
[14]	Umeda J, Sano S, Kogawa K, et al. In vivo cooperation between Bcl-xL and the phosphoinositide 3-kinase-Akt signaling pathway for the protection of epidermal kerafinoeytes from apoptosis[J].FASEB J, 2003, 17(6):610-620.
[15]	Dunn IF, Heese O, Black PM, et al. Growth factors in glioma angiogenesis:FGFs, PDGF, EGF and TGFs[J]. J Neuro Oncol, 2000,50(1-2):121-137.
[16]	周颖奇,王智巍,王承,等.中国人胶质瘤中表皮生长因子受体基因的扩增及对患者预后的影响[J].中华神经外科杂志,2003,19(1):26-29.
[17]	Chakravarti A, Loeffler JS, Dyson N J, et al. Insulin-like growth factor receptor I mediates resistance to anti-epidermal growth factor receptor therapy in primary human glioblastoma cells through continued activation of phosphoinositide 3-kinase signaling[J]. Cancer Res, 2002, 62(1):200-207.
[18]	Chakravarti A, Chakladar A, Delaney MA, et al. The epidermal growth factor receptor pathway mediates resistance to sequential administration of radiation and chemotherapy in primary human glioblastoma cells in a RAS-dependent manner[J]. Cancer Res,2002, 62(15):4307-4315.
[19]	Gomez Del Pulgar T, De Ceballos ML. Cannabinoids protect astrocytes from ceramide-induced apoptosis through the phosphatidylinositol 3-kinase/protein kinase B pathway[J]. J Biol Chem, 2002,277(39):36527-36533.
[20]	Alphonse G, Aloy MT, Broquet P, et al. Ceramide induces activation of the mitochondrial/caspases pathway in Jurkat and SCC61 cells sensitive to gamma-radiation but activation of this sequence is defective in radioresistant SQ20B ceils[J]. Int J Radiat Biol, 2002,78(9):821-835.
[21]	Michael JM, Lavin MF, Watters DJ, et al. Resistance to radiation-induced apoptosis in Burki's lymphoma cells is associated with defective ceramide signaling[J]. Cancer Res, 1997, 57(16):3600-3605.
[22]	Kubota N, Okada S, Inada T, et al. Wortmannin sensitizes human glioblastoma cell lines carrying mutant and wild type TP53 gene to radiation[J]. Cancer Letter, 2000, 161(2):141-147.
[23]	Okada S, Ono K, Hamada N, et al. A low-pH culture condition enhances the radiosensitizing effect of wortmannin[J], Int J Ⅱ JRadiat Oncol Biol Phys, 2001, 49(4):1149-1156.
[24]	Okaichi K, Suzuki K, Morita N, et al. Low dose of wortmannin reduces radiosensitivity of human glioblastoma cells through the p53 pathway[J]. Oncol Report, 2002, 9(4):859-862.

[1]	刘影 , 李传福 . 功能性磁共振成像在胶质瘤中的应用. 国际放射医学核医学杂志, 2005, 29(3): 143-145.
[2]	高云朝 . 恶性胶质瘤的放射免疫治疗. 国际放射医学核医学杂志, 2004, 28(4): 149-152.
[3]	宁静 , 于鹏 , 刘家金 , 党浩丹 , 徐白萱 . ¹⁸F-FDG PET/CT图像的影像组学分析在胶质瘤MGMT基因甲基化状态评估中的初步应用. 国际放射医学核医学杂志, 2020, 44(8): 486-492. doi: 10.3760/cma.j.cn121381-201903057-00064
[4]	储小飞 , 赵舒怡 , 樊赛军 . 肿瘤干细胞与辐射抗性的研究进展. 国际放射医学核医学杂志, 2015, 39(5): 431-436. doi: 10.3760/cma.j.issn.1673-4114.2015.05.019
[5]	严惟力 , 黄钢 . 乳腺癌辐射抗性的影响因素及其可能作用. 国际放射医学核医学杂志, 2006, 30(4): 193-195.
[6]	焦圣元 , 高巧慧 , 达飞 , 郭利 , 王晋 , 郭娟 , 李静 , 刘军叶 . 缺氧诱导的UCHL5增强宫颈癌Hela细胞辐射抗性. 国际放射医学核医学杂志, 2021, 45(1): 31-40. doi: 10.3760/cma.j.cn121381-202010021-000011
[7]	朱长春 , 冯国兴 , 董佳丽 , 姜勉 , 贺俊博 , 樊赛军 . 应用生物信息学确定结直肠癌辐射抗性细胞的差异表达基因. 国际放射医学核医学杂志, 2018, 42(4): 340-345, 351. doi: 10.3760/cma.j.issn.1673-4114.2018.04.010
[8]	陈剑 , 刘芬菊 . 抗辐射球菌辐射抗性机制的研究. 国际放射医学核医学杂志, 2003, 27(5): 225-227.
[9]	丁立 , 金一尊 . 人恶性神经胶质瘤的辐射敏感性试验. 国际放射医学核医学杂志, 1993, 17(3): 119-119.
[10]	王洗 , 刘强 . 脑胶质瘤辐射敏感性相关基因的研究进展. 国际放射医学核医学杂志, 2008, 32(5): 311-313.

点击查看大图

计量

文章访问数: 1067
HTML全文浏览量: 96
PDF下载量: 2

PI3K/Akt与胶质瘤辐射抗性

薛景
刘芬菊

215006 苏州, 苏州大学放射医学与公共卫生学院

收稿日期: 2004-10-08

基金项目: 苏州大学医学发展基金重点项目资助(EE126031)

关键词:

PI3K/Akt /
胶质瘤 /
辐射抗性

摘要: 恶性脑胶质瘤的术后治疗是患者预后生存期延长的关键,如何提高肿瘤组织的辐射敏感性,增强正常组织的辐射抗性是当前肿瘤放射生物学及临床放疗研究的热点。研究资料表明,PI3K/Akt抗细胞凋亡通路的激活提高了部分细胞的辐射抗性,特别在表皮细胞受紫外线照射的研究中提示,辐射产生的活性氧可能是该通路激活的原因之一;电离辐射可能诱导相关的细胞因子通过激活PI3K/Akt通路介导胶质瘤细胞的辐射抗性;PI3K及其相关酶可能通过DNA修复途径发挥抗辐射作用。PI3K/Akt通路的研究可为放射治疗胶质瘤提供新型的增敏药。