期刊文献+

过表达Axin对胶质瘤细胞U87的生物学行为的影响及其作用机制

The effect of over-expression of Axin on the biological behavior of glioma U87 cells and its mechanism
下载PDF
导出
摘要 目的:观察Axin对胶质瘤U87细胞生物学行为的影响,并探讨其机制。方法:pCMV5-HA-Axin瞬时转染胶质瘤U87细胞,TUNEL法检测细胞的凋亡,流式细胞仪检测瘤细胞周期变化,Western blot检测Axin及β-catenin蛋白质的表达。结果:Axin显著促进胶质瘤U87细胞的凋亡、抑制细胞的增殖;促进β-catenin蛋白在胞浆内的蓄积。结论:过表达Axin的胶质瘤U87细胞可能通过降低细胞核内β-catenin的蛋白表达量抑制Wnt信号通路,从而抑制细胞增殖并促使细胞凋亡。 Objective: To investigate the effect of Axin on the biological behavior of U87 cells of glioma and to elu cidate its molecular mechanism. Methods: U87 cells of glioma were transfered with pCMV5 HA Axin. The cell proliferation was detected by flow cytometry and the apoptosis was analyzed by TUNEL assay. At the same time, Western blot was used to detect the expression of Axin and β catenin in U87 cells. Results: Over expression of Ax in inhibited significantly the growth of U87 cells. Axin increased the proportion of cytoplasmic β catenin. Conclu sion: Over expression of Axin might inhibit the activity of Wnt signaling pathway by decreasing nuclear β catenin, and its over expression can inhibit the proliferation and induce the apoptosis of U87 ceils.
出处 《现代肿瘤医学》 CAS 2014年第7期1507-1510,共4页 Journal of Modern Oncology
基金 肿瘤生物学国家重点实验室开放基金项目(编号:CBSKL 2005004)
关键词 胶质瘤 AXIN β—catenin 细胞增殖 细胞凋亡 glioma Axin β - catenin proliferation apoptosis
  • 相关文献

参考文献2

二级参考文献11

  • 1[1]Zeng L, Fagotto F, Zhang T, et al. The mouse Fused locus encodes Axin, an inhibitor of the Wnt signaling pathway that regulates embryonic axis formation [J]. Cell, 1997, 90( 1 ): 181 - 192.
  • 2[2]Satoh S, Daigo Y, Furukawa Y, et al. AXIN1 mutations in hepatocellular carcinomas, and growth suppression in cancer cells by virus-mediated transfer of AXIN1 [J]. Nat Genet, 2000, 24(3): 245- 250.
  • 3[3]Budowle B, Chakraborty R, Giusti AM, et al. Analysis of the VNTR locus D1 S80 by the PCR followed by high-resolution PAGE [ J]. Am J Hum Genet, 1991, 48(1): 137-144.
  • 4[4]Jho E, Lomvardas S, Costantini F. A GSK3beta phosphorylation site in axin modulates interaction with beta-catenin and Tcf-mediated gene expression [ J]. Biochem Biophys Res Commun, 1999, 266( 1 ): 28 -35.
  • 5[5]Fagotto F, Jho E, Zeng L, et al. Domains of axin involved in proteinprotein interactions, Wnt pathway inhibition, and intracellular localization [J]. J Cell Biol, 1999, 145(4):741-756.
  • 6[6]Zhang Y, Qiu WJ, Liu DX, et al. Differential molecular assemblies underlie the dual function of Axin in modulating the WNT and JNK pathways [J]. J Biol Chem, 2001, 276(34): 32152-32159.
  • 7[7]Webster MT, Rozycka M, Sara E, et al. Sequence variants of the axin gene in breast, colon, and other cancers: an analysis of mutations that interfere with GSK3 binding [J]. Genes Chromosomes Cancer, 2000,28(4): 443 -453.
  • 8[8]Dahmen RP, Koch A, Denkhaus D, et al. Deletions of AXIN1, a component of the WNT/wingless pathway, in sporadic medulloblastomas [J]. Cancer Res, 2001, 61(19): 7039-7043.
  • 9[9]Miao J, Kusafuka T, Udatsu Y, et al. Axin, the main component of the Wnt signaling pathway, is not mutated in kidney tumors in children [J]. Int J Mol Med, 2002, 9(4): 377 -379.
  • 10[10]Sakanaka C, Williams LT. Functional domains of axin. Importance of the C terminus as an oligomerization domain [ J]. J Biol Chem, 1999,274(20): 14090 - 14093.

共引文献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