期刊文献+

Stat3反义核苷酸通过调节凋亡相关因子诱导喉癌细胞凋亡 被引量:3

Stat3 antisense oligodeoxynucleotide induces apoptosis in laryngeal carcinoma cells by regulating apoptosis-related factors
原文传递
导出
摘要 目的:探讨反义Stat3基因诱导喉癌细胞凋亡的机制。方法:将设计好的已证实能诱导人喉癌细胞凋亡的Stat3反义寡核苷酸序列,应用脂质体瞬时转染法转染人喉癌Hep-2细胞,应用Western blot、PCR检测Hep-2细胞中Bcl-2,Bax及C-Myc基因及蛋白的表达情况。结果:Western blot和RT-PCR结果显示转染Stat3反义寡核苷酸细胞组,Bax的表达随反义寡核苷酸浓度增加,表达增强,而Bcl-2及C-Myc的表达则减弱。结论:反义Stat3寡核苷酸通过上调Bax,下调Bcl-2及C-Myc基因表达来参与其诱导人喉癌Hep-2细胞凋亡的过程。 Objective:To study the mechanism of apoptosis in laryngeal carcinoma cell induced by Stat3 antisense oligodeoxynucleotide (ASODN).Method:The designed Stat3 ASODN was transferred into laryngeal cacinoma Hep-2 cell by lipofection. Expression of Bcl-2,Bax and C-Myc were detected by Western blot and PCR.Result:Western blot and PCR results demonstrated that Stat3 ASODN could significantly increased the expression of Bax and decreased the expression of Bcl-2 and C-Myc when the concentration of antisense oligodeoxynucleotide were heightened.Conclusion:Stat3 ASODN participate in apoptosis by enhancing the expression of Bax and reducing the expression of Bcl-2 and C-Myc.
出处 《临床耳鼻咽喉头颈外科杂志》 CAS CSCD 北大核心 2010年第4期155-157,共3页 Journal of Clinical Otorhinolaryngology Head And Neck Surgery
关键词 喉肿瘤 反义寡脱氧核苷酸 STAT3 凋亡机制 laryngeal neoplasms antisense oligodeoxynucleotide Stat3 apoptosis mechanism
  • 相关文献

参考文献8

  • 1FERNANDES A, HAMBURGER A W, GERWIN B I. ErbB-2 kinase is required for constitutive stat3 activation in malignant human lung epithelial cells[J]. Int J Cancer, 1999,83 : 564- 570.
  • 2BROMBERG J F, WRZESZCZYNSKA M H, DEV GAN G, et al. Stat3 as an oncogene[J].Cell, 1999, 98:295-303.
  • 3YU H, JOVE R. The STATs of cancer new molec- ular targets come of age[J].Nat Rev Cancer,2004,4: 97-105.
  • 4吕海丽,张秋航,严波.Stat3反义寡脱氧核苷酸在体外诱导喉癌细胞凋亡[J].临床耳鼻咽喉头颈外科杂志,2008,22(21):968-971. 被引量:6
  • 5GROEGER A M, ESPOSITO V, DE LUCA A, et al. Prognostic value of immunohistochemical expression of p53, bax, Bcl-2 and Bcl-xL in resected non- small-cell lung cancers[J]. Histopathology, 2004, 44:54-63.
  • 6GOBEG,RUBIN M, WIIAAAMS G, et al. Apoptosis and expression of Bcl-2, Bcl-xL, and Bax in renal cell carcinomas[J]. Cancer Invest, 2002,20 : 324 - 332.
  • 7OLTVAI Z N, MILLIMAN C L, KORSMEYER SJ Bcl-2 heterodimerizes in vivo with a conserved homo log,Bax, that accelerates programmed cell death[J].Cell, 1993,74 :609-619.
  • 8KIUCHI N, NAKAJIMA K, ICHIBA M, et al. ST- AT3 is required for the gp130-mediated full activation of the c-myc gene[J]. J Exp Med,1999,189:63-73.

二级参考文献1

共引文献5

同被引文献22

  • 1唐古生,蔡建明,倪瑾,项莺松,崔建国,朱丹,董俊瑞.反义STAT3对肿瘤细胞增殖抑制和诱导凋亡的作用[J].癌症,2006,25(3):269-274. 被引量:18
  • 2GALMICHE A,RASSOW J,DOYE A,et al.TheN-terminal 34kDa fragment of Helicobacter pylorivacuolating cytotoxin targets mitochondria and inducescytochrome c release[J].EMBO J,2000,19:6361-6370.
  • 3GREEN D R,KROEMER G.The pathophysiology ofmitochondrial cell death[J].Science,2004,305:626-629.
  • 4BOSSY-WETZEL E,NEWMEYER D D,GREEN DR.Mitochondrial cytochrome c release in apoptosisoccurs upstream of DEVD-specific caspase activationand independently of mitochondrial transmembrancedepolarization[J].EMBO J,1998,17:37-49.
  • 5PASTORINO J G,SHULGA N,HOEK J B.Mito-chondrial binding of hexokinaseⅡinhibits Bax-inducedcytochrome c release and apoptosis[J].J Biol Chem,2002,277:7610-7618.
  • 6SHIMIZU S,SHINOHARA Y,TSUJIMOTO Y.Bax and Bcl-xL independently regulate apoptotic chan-ges of yeast mitochondria that require VDAC but notadenine nucleotide translocator[J].Oncogene,2000,19:4309-4318.
  • 7GRUZ P,PISARI F M,SHIMIZU M,et al.Syn-thetic activity of Sso DNA polymerase Y1,an archaelDinB-like DNA polymerase,is stimulated by proces-sivity factors proliferating cell nuclear antigen and rep-lication factor C[J].J Biol Chem,2001,276:47394-47401.
  • 8Shukla S, Shishodia G, Mahata S, et al. Aberrant expression and constitutive activation of STAT3 in cervical carcinogenesis: implications in high-risk human papillomaviras infection [ J]. Mol Cancer,2010,9:282 - 298.
  • 9Kortylewski M, Yu H. Stat3 as a potential target for cancer immunotherapy [ J ]. J Immunother,2007,30 ( 2 ) : 131 - 139.
  • 10Han Z, Hong Z, Chen C, et al. A novel oncolytic adenovirus selectively silences the expression of tumor-associated STAT3 and exhibits potent antitumoral activity [ J ]. Carcinogenesis, 2009, 30(12) :2014 -2022.

引证文献3

二级引证文献6

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