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结肠癌获得性肿瘤坏死因子相关凋亡诱导配体基因耐药机制 被引量：2

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摘要 肿瘤坏死因子相关凋亡诱导配体（TRAIL）能杀灭众多肿瘤细胞而不损伤多数正常细胞,它的发现为肿瘤基因治疗带来了新的曙光,但深入研究发现,TRAIL基因治疗的进一步发展受到了耐药问题的困扰.了解TRAIL基因耐药机制,尤其是治疗过程中形成的获得性耐药机制,对于预防并逆转耐药具有重要意义.
作者 朱洪波 陈琳琳 何超 毛伟芳 黄学锋
机构地区 浙江大学医学院附属邵逸夫医院肛肠外科及临床医学研究所
出处 《中华消化杂志》 CAS CSCD 北大核心 2006年第6期404-405,共2页 Chinese Journal of Digestion
基金 国家自然科学基金资助项目(30271467)
关键词 肿瘤坏死因子相关凋亡诱导配体 肿瘤基因治疗 耐药机制 获得性 TRAIL基因 结肠癌 正常细胞 肿瘤细胞 研究发现 治疗过程
分类号 R735.35 [医药卫生—肿瘤]
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参考文献5

  • 1Zhang L,Fang B.Mechanisms of resistance to TRAIL-induced apoptosis in cancer.Cancer Gene Ther,2005,12:228-237.
  • 2Zhang L,Gu J,Lin T,et al.Mechanisms involved in development of resistance to adenovirus-mediated proapoptotic gene therapy in DLD-1 human colon cancer cell line.Gene Ther,2002,9:1262-1270.
  • 3Hinz S,Trauzold A,Boenicke L,et al.Bcl-XL protects pancreatic adenocarcinoma cells against CD95-and TRAIL receptormediated apoptosis.Oncogene,2000,19:5477-5486.
  • 4Muhlethaler-Mottet A,Bourloud KB,Auderset K,et al.Drugmediated sensitization to TRAIL-induced apoptosis in caspase-8complemented neuroblastoma cells proceeds via activation of intrinsic and extrinsic pathways and caspase-dependent cleavage of XIAP,Bcl-xL and RIP.Oncogene,2004,23:5415-5425.
  • 5Yang X,Merchant MS,Romero ME,et al.Induction of caspase-8 by interferon gamma reders some neuroblastoma (NB) cells sensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) but reveals that a lack of membrane TR1/TR2 also contributes to TRAIL resistance in NB.Cancer Res,2003,63:1122-1129.

同被引文献14

  • 1朱洪波,朱玉萍,黄学锋,何超,毛伟芳.Bcl-XL小分子干扰RNA在结肠癌氟尿嘧啶耐药细胞中的治疗作用[J].中华消化杂志,2006,26(4):272-274. 被引量：7
  • 2Johnstone RW, Frew AJ, Smyth MJ. The TRAIL apoptotic pathway in cancer onset, progression and therapy [ J]. Nat Rev Cancer, 2008,8(10) :782-798.
  • 3Thorburn A, Behbakht K, Ford H. TRAIL receptor-targeted therapeutics: resistance mechanisms and strategies to avoid them[ J]. Drug Resist Updat ,2008,11 ( 1-2 ) : 17-24.
  • 4Johnson TR, Stone K, Nikrad M, et al. The proteasome inhibitor PS-341 overcomes TRAIL resistance in Bax and easpase 9-negative or Bcl-xL overexpressing cells [ J ]. Oncogene, 2003, 22 ( 32 ) : 4953-4963.
  • 5Sayers T J, Brooks AD, Koh CY, et al. The proteasome inhibitor PS-341 sensitizes neoplastic ceils to TRAIL-mediated apoptosis by reducing levels of c-FLIP[ J]. Blood, 2003, 102( 1 ) :303-310.
  • 6Dai Y, Rahmani M, Grant S. Proteasome inhibitors potentiate leukemic cell apoptosis induced by the cyclin-dependent kinase inhibitor flavopiridol through a SAPK/JNK- and NF-kappaB-dependent process[J]. Oncogene, 2003, 22(46): 7108-7122.
  • 7Lashinger LM, Zhu K, Williams SA, et al. MG-132 abolishes tumor necrosis factor-related apoptosis-inducing ligand resistance via a p21-dependent mechanism in human bladder and prostate cancer cells[J]. Cancer Res, 2005, 65( 11 ) : 4902-4908.
  • 8Zhu H, Zhang L, Dong F, et al. Bik/NBK accumulation correlates with apoptosis-induction by MG-132 (PS-341 ,Velcade) and other proteasome inhibitors[ J]. Oncogene, 2005,24(31) : 4993-4999.
  • 9Chen LF, Greene WC. Shaping the nuclear action of NF-kappaB [J]. Nat Rev Mol Cell Biol, 2004, 5(5) : 392-401.
  • 10An J, Sun Y, Fisher M, et al. Maximal apoptosis of renal cell carcinoma by the proteasome inhibitor bortezomib is nuclear factor- B dependent[J]. Mol Cancer Ther, 2004, 3(6): 727-736.

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中华消化杂志
2006年 第6期

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