期刊文献+

DcR3在喉癌组织中的表达及其与细胞凋亡相关性的研究 被引量:1

原文传递
导出
摘要 目的探讨诱骗受体(decoy receptor3,DcR3)在喉癌组织中的表达及其与细胞凋亡相关性。方法采用流式细胞术检测41例喉癌组织及其相应癌旁组织中的DcR3的表达,并以15例非喉癌患者喉部正常黏膜组织作对照;同时检测喉癌组织中的细胞凋亡率。结果喉癌组织中DcR3蛋白的表达量明显高于癌旁组织及正常喉黏膜组织(F=27.07,P〈0.05),癌旁组织及正常喉黏膜组织的表达无差别(P〉0.05)。DcR3蛋白的表达与喉癌组织中的淋巴转移、临床分期、分化程度有关(P〈0.05);与临床分型、肿瘤大小、吸烟量、年龄和性别无关(P〉0.05)。喉癌组织细胞凋亡率与临床分期、淋巴转移有关;与临床分型、病理分级、肿瘤大小、吸烟量、年龄和性别无关。喉癌组织中DcR3蛋白表达水平与喉癌组织细胞凋亡率呈负相关。结论DcR3蛋白的高表达可促进喉癌的发生、发展,并通过抑制凋亡并促进细胞增殖参与喉癌发展。
出处 《中华耳鼻咽喉头颈外科杂志》 CAS CSCD 北大核心 2009年第8期691-693,共3页 Chinese Journal of Otorhinolaryngology Head and Neck Surgery
  • 相关文献

参考文献3

二级参考文献16

  • 1Xiong H Q.Molecular targeting therapy for pancreaticcancer[].Cancer Chemotherapy and Pharmacology.2004
  • 2Lin J C,Chang S Y,Hsieh D S et al.Modulation of mito- gen-activated protein kinase cascades by differentiation-1 protein: acquired drug resistance of hormone independent prostate cancer cells[].J Urol.2005
  • 3Habiro A,Tanno S,Koizumi K et al.Involvement of p38 mitogen-activated protein kinase in gemcitabine-induced apoptosis in human pancreatic cancer cells[].Biochem Biophys Res Commun.2004
  • 4Kohno M,Pouyssegur J.Pharmacological inhibitors of the ERK signaling pathway: application as anticancer drugs[].Prog Cell Cycle Res.2003
  • 5English JM,Cobb MH.Pharmacological inhibitors of MAPK pathways[].Trends in Pharmacological Sciences.2002
  • 6Park MT,Choi JA,Kim MJ,et al.Suppression of extracellular signal-related kinase and activation of p38 MAPK are two critical events leading to caspase-8 and mitochondria-mediated cell death in phytosphingosine-treated human cancer cells[].Journal of Biological Chemistry.2003
  • 7FESIK SW.Promoting apoptosis as a strategy for cancer drug discovery[].Nature Reviews Cancer.2005
  • 8Wada T,Penninger JM.Mitogen-activated protein kinases in apoptosis regulation[].Oncegene.2004
  • 9Dent P,Yacoub A,Fisher P B,Hagan M P,Grant S.MAPK pathways in radiation responses[].Oncegene.2003
  • 10Sanchez-Prieto R,Rojas JM,Taya Y,Gutkind JS.A role for the p38 mitogen-activated protein kinase pathway in the transcriptional activation of p53 on genotoxic stress by chemotherapeutic agents[].Cancer Research.2000

共引文献46

同被引文献10

  • 1Pitti RM,Marsters SA,Lawrence DA,et al.Genomic ampli-fication of a decoy receptor for Fas ligand in lung and colon cancer[J].Nature,1998,396(6712):699.
  • 2Yang CR,Hsieh SL,Teng CM,et al.Soluble decoy receptor3 induces angiogenesis by neutralization of TL1A,a cytokine be-longing to tumor necrosis factor superfamily and exhibiting angio-static action[J].Cancer Res,2004,64(3):1122.
  • 3Gill RM,Hunt JS.Soluble receptor(DcR3)and cellular in-hibitor of apoptosis-2(clap-2)protect human cytotrophoblastcells against LIGHT-mediated apoptosis[J].Am J Palhol,2004,165(1):309.
  • 4Bai C,Connolly B,Metzker ML,et al.Overexpression ofM68/DcR3 in human gastrointestinal tract tumors independent ofgene amplification and its location in a four-gene cluster[J].Proc Natl Acad Sci USA,2000,97(3):1230.
  • 5Sinicropo FA,Ruan SB,Cleary KR,et al.Bcl-2and p53oncoprotein expression during colorectal tumorigenesis[J].CancerRes,1995,55(2):237.
  • 6Connor JP,Felder M.Ascites from epithelial ovarian cancercontain high levels of functional decoy receptor 3(DcR3)and isassociated with platinum resistance[J].Gynecol Oncol,2008,111(2):330.
  • 7Macher-Goeppinger S,Aulmann S,Wagener N,etal.Decoy receptor 3 is a prognostic factor in renal cell cancer[J].Neoplasia,2008,10(10):1049.
  • 8Chang PM,Chen PM,Hsieh SL,et al.Expression of a solu-ble decoy receptor 3 in patients with diffuse large B-cell lympho-ma predicts clinical outcome[J].Int J Oncol,2008,33(3):549.
  • 9Ho CH,Chen CL,Li WY,et al.Decoy receptor3,upregu-lated by Epstein-Barr virus latent membrane protein 1,enhancesnasopharyngeal carcinoma cell migration and invasion[J].Carci-nogenesis,2009,30(8):1443.
  • 10Takahama Y,Yamada Y,Emoto K,et al.The prognosticsignificance of over expression of the decay receptor for fas ligand(DcR3)in patients with gastric carcinomas[J].Gastric Cancer,2002,5(2):61.

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部