期刊文献+

上皮生长因子受体-信号转导与转录激活因子3信号转导通路与喉乳头状瘤的相关性研究 被引量:2

Study on the correlation between EGFR-STAT3 signal pathway and laryngeal papilloma
原文传递
导出
摘要 目的:探讨喉乳头状瘤中上皮生长因子受体(EGFR)和信号转导与转录激活因子3(STAT3)的表达与其生物学行为的关系。方法:采用RT-PCR、免疫组织化学方法和Westernblot,检测42例喉乳头状瘤和15例正常喉黏膜组织中EGFR和STAT3、磷酸化-STAT3(p-STAT3)的mRNA和蛋白质表达情况,同时将蛋白质表达水平与喉乳头状瘤的临床病理参数进行相关性分析。结果:EGFR与STAT3的mRNA在喉乳头状瘤组织表达水平显著高于正常喉组织(P<0.05,P<0.01)。免疫组织化学及Westernblot方法也证实喉乳头状瘤组织中EGFR与STAT3(p-STAT3)的蛋白质表达水平显著高于正常喉组织(P<0.05)。EGFR与STAT3(p-STAT3)蛋白质在喉乳头状瘤组织的表达显著关联(P<0.05),STAT3蛋白与喉乳头状瘤的复发和恶变有明显相关性(P<0.05)。结论:EGFR-STAT3信号转导通路参与喉乳头状瘤的发生,STAT3蛋白的持续活化可能促进喉乳头状瘤的复发与恶变。 Objective:To explore the relationship between the expression of EGFR and STAT3 in human laryngeal papilloma and its biological behavior. Method:Reverse transcription polymerasechain reaction(RT-PCR), immunohistochemical staining and Western blot were used to evaluate the mRNA and protein expression of EGFR and STAT3(p-STAT3) in 42 laryngeal papilloma tissues and 15 samples of normal laryngeal tissue, and the relationship between the protein expression of them and clinicpathological parameters was also analysized. Result: The mRNA expression levels of EGFR and STAT3 in laryngeal papilloma tissue were significantly higher than that in normal laryngeal tissue(P〈0.05 ,P〈0.01). Protein positive expression of EGFR and p-STAT3 were also detected in a significantly greater proportion of laryngeal papilloma than normal laryngeal tissue by immunohistochemistry and western blot(P〈(0.01 ,P〈0. 05). There was relationship between EGFR and p-STAT3 overexpression in laryngeal papilloma(P〈0.05). The expression p-STAT3 was correlated with the recurrence and canceration of laryngeal papilloma(P〈0.05). Conclusion: The EGFR-STAT3 signal transduction pathway may be involved in the pathogenesis of laryngeal papilloma,, and the persistent activation of STAT3 gene plays an important role in the recurrence and canceration of laryngeal papilloma.
出处 《临床耳鼻咽喉头颈外科杂志》 CAS CSCD 北大核心 2009年第18期832-836,共5页 Journal of Clinical Otorhinolaryngology Head And Neck Surgery
关键词 喉乳头状瘤 信号转导通路 上皮生长因子受体 信号转导与转录激活因子3 laryngeal papilloma signal transduction pathway epidermal growth factor receptor signal transducer and activator of transcription3
  • 相关文献

参考文献11

  • 1CHAN K S,CABAJAL S,KIGUCHI K,et al. Epidermal growth factor receptor-mediated activation of Stat3 during multistage skin carcinogenesis[J].Cancer Res, 2004,64 : 2382- 2389.
  • 2王伯法 李玉松 黄高升 张远强.病理学技术[M].北京:人民卫生出版社,2000.393.
  • 3FORD A C, GRANDIS J R. Targeting epidermal growth factor receptorin head and neck caneer[J].Head Neck,2003,25:67-73.
  • 4RUBIN G J, ZENG Q, DRENNING S D. Epidermal growth factor recepmediated slat3 signaling blocks apoptosis in head and neck cancer [J].Laryngoscope, 2000,110 :868-874.
  • 5GRANDIS J R, DRENNING S D,CHAKRABOXTY A,et al. Requirementof Stat3 but not Statl activation for epidermal growth factor receptor-mediated cell growth in vitro[J]. J Clin Invest, 1998,102: 1385- 1392.
  • 6张铁松,林建云,赵生全,高映勤,周丽娟,刘睿清.儿童喉乳头状瘤与人乳头状瘤病毒的相关性及其免疫综合治疗[J].临床耳鼻咽喉科杂志,2006,20(21):993-995. 被引量:5
  • 7JOHNSTON D, HALL H, DILORENZO T P,et al. Elevation of the epidermal growth factor receptor and dependent signaling in human papilloma virus-infected laryngeal papillomas[J]. Cancer Res, 1999,59 :968- 974.
  • 8WU R, ABRAMSON A L, SHIKOWITZ M J,et al. Epidermal growth factor-induced cyclooxygenase-2 expression is mediated through phosphatidylinositol-3 kinase, not mitogen-activated protein/extracellular signal-regulated kinase kinase, in recurrent respiratory papillomas[J]. Clin Cancer Res, 2005, 11: 6155- 6161.
  • 9JING N, ZHU Q, YUAN P,et al. Targeting signal transducer and activator of transcription 3 with G- quartet oligonucleotides., a potential novel therapy for head and neck cancer[J]. Mol Cancer Ther, 2006,5: 279-286.
  • 10WU R, SUN S, STEINBERG B M. Requirement of STAT 3 activation for differentiation of mucosal stratified squamous epithelium[J]. Mol Med,2003,9 : 77- 84.

二级参考文献4

共引文献82

同被引文献18

  • 1Shyhon M, Kuo.M, Pearman K. Recurrent respiratory papillomatosis[ J]. Clin OtolaIyngol Allied Sci ,2002,27:237 - 243.
  • 2Lin HW, Richmon JD, Emerick KS. Malignant transformation of a highly aggressive human papillomavirus type 11-associated recurrent respiratory papillomatosis. [ J ]. Am J Otolaryngol,2009 ,7 :9.
  • 3Draganov P, Todorov S, Todorov S, et al. Identification of HPV DNA in patients with juvenile-onset recurrent respiratory papillomatosis using SYBR Green real-time PCR [J]. Int J Pediatr Otorhinolaryn- go1,2006,70 ( 3 ) :469 - 73.
  • 4Kimberlin DW, Malis DJ. Juvenile onset recurrent respiratory papillomatosis:possibilities for successful antiviral therapy [ J ]. Antiviral Res, 2000,45:83 - 93.
  • 5Valerie A, Yanrsos MD, Gist H. Recurrent Juvenile-Onset Laryngotracheal Papillomatosis With Transformation to Squamous Cell Carcinoma of the Lung [ J ]. Southern Medical Journal, 1999,92 ( 10 ) : 1013 -1016.
  • 6Selvakumar R, Borenstein LA, Lin YL, et al. Immunization with nonstructural proteins E1 and E2 of cottontail rabbit papillomavirus stimulates regression of virus-induced papillomas [ J]. J Virol, 1995,69:602 - 605.
  • 7Selvakumar R, Schmitt A, Iftner T, et al. Regression of papillomas induced by cottontail rabbit papillomavirus is associated with infiltration of CD8 + cells and persistence of viral DNA after regression [J]. J Virol,1997,71:5540 -5548.
  • 8Gelder CM, Williams OM, Hart KW, etal. HLA classlI polymor- phisms and susceptibility to recurrent respiratory papillomatosis[ J]. Viro1,2003 ,7 :927 - 939.
  • 9Williams OM, Hart KW, Wang EC, Gelder CM:Analysis of CIM ( + )T-cell responses to human papillomavirus (HPV)typell Ll in healthy adults reveals a high degree of responsiveness and cross-reactivity with other HPV types [ J ]. Viro1,2002,76 : 18 - 29.
  • 10Lele SM,Pou AM, Ventura K, et al. Molecular events in the progression of recurrent respiratory papillomatosis to carcinoma [ J ]. Arch Pathol Lab Med ,2002 ,126 : 1184 - 1188.

引证文献2

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