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转化生长因子-β受体Ⅲ在胶质瘤组织中的表达及意义 被引量:1

Expression and significance of TβRⅢ in tissue of human glioma
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摘要 目的探讨转化生长因子-β受体Ⅲ(TβRⅢ)在胶质瘤发生发展中的作用。方法采用免疫组化法检测TβRⅢ在3例正常脑组织、13例低级别(Ⅰ、Ⅱ级)胶质瘤和27例高级别(Ⅲ、Ⅳ级)胶质瘤中的表达,Western Blot法进一步验证各级别不同病理类型中TβRⅢ表达。结果正常脑组织中TβRⅢ阳性表达率为100%(3/3),低级别胶质瘤阳性表达率为84.6%(11/13),高级别胶质瘤阳性表达率为48.1%(13/27),高、低级别间比较,P<0.05;Ⅱ、Ⅲ级肿瘤中,星形细胞瘤和含少突成分的胶质瘤间TβRⅢ的表达无显著差异。结论高级别胶质瘤中TβRⅢ表达降低;TβRⅢ可能参与了胶质瘤的恶变过程,其低表达可促进肿瘤的侵袭和迁移。 Objective To investigate the roles of transforming growth factor-β receptor m (TβRⅢ) in the occurrence and development of human glioma. Methods Immunohistochemistry and western blot were used to detect the differential expression of TβRⅢ in 3 normal brain tissues, 13 low-grade gliomas and 27 high-grade gliomas. Results TβRⅢ in 3 normal brain tissues all presented positive expression, which was 84.6% in 13 low-grade gliomas and 48.1% in 27 high- grade gliomas (P 〈 0.05). However, there was no significance differential expression between astrocytoma and glioma with oligodendroglioma in Ⅱ and Ⅲ grade. Conclusion The low expression of TβRⅢ in high-grade gliomas may have important roles in the neoplastic processes by promoting the invasion and migration of glioma.
出处 《山东医药》 CAS 2012年第39期32-34,共3页 Shandong Medical Journal
基金 天津市应用基础及前沿技术研究计划(11JCYBJC12100)
关键词 神经胶质瘤 受体 转化生长因子β免疫组织化学 印迹法 蛋白质 glioma receptors, transforming growth factor beta immunohistochemistry Westernblotting protein
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  • 1Turley RS, Finger EC, Hempel N, et al. The type I transforming growth factor-beta receptor as a novel tumor suppressor gene in prostate cancer[ J]. Cancer Res, 2007,67 (3) : 1090-1098.
  • 2于士柱,孙翠云.中枢神经系统肿瘤病理学的十年进展[J].中国现代神经疾病杂志,2010,10(1):137-141. 被引量:7
  • 3王岸柳,张力伟,刘朝霞,李光,林松.PTEN和EGFR蛋白在人脑胶质瘤中的表达及意义[J].山东医药,2010,50(39):23-24. 被引量:5
  • 4You H J, How T, Blobe GC. The type III transforming growth fac- tor-beta receptor negatively regulates nuclear factor kappa B signa- ling through its interaction with beta-arrestin2 [ J ]. Carcinogenesis, 2009,30 ( 8 ) : 1281-1287.

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  • 1魏强,王健伟,郭丽,屈建国,赵玉琪,洪涛.以人甲胎蛋白启动子控制表达HIV-1vpr基因的重组腺病毒诱导肝癌细胞G2期阻滞和细胞凋亡作用的研究[J].中国实验诊断学,2006,10(7):725-729. 被引量:2
  • 2Wen X, Duus KM, Friedrich TD, et al. The HIV1 protein Vpr acts to promote G2 cell cycle arrest by engaging a DDB1 and Cullin4A-containing ubiquitin ligase complex using VprBP/DCAF1 as an adaptor[J]. J Biol Chem,2007,282:27046-27057.
  • 3Planelles V, Benichou S. Vpr and its interactions with cellular proteins [ J ]. Curr Top Microbiol Immuno1,2009,339 : 177-200.
  • 4Ma B, Zhang H, Wang J, et al. HIV-1 viral protein R (Vpr) induction of apoptosis and cell cycle arrest in multidrug-resistant colorectal cancer cells [ J ]. Oncol Rep, 2012, 28:358-364.
  • 5Huard S, Eider RT, Liang D, et al. Human immunodeficiency virus type 1 Vpr induces cell cycle G2 arrest through Srkl/MK2- mediated phosphorylation of Cdc25 [ J ] . J Virol, 2008, 82: 2904 -2917.
  • 6Matsuda N, Tanaka H, Yamazaki S, et al. HIV-1 Vpr induces G2 cell cycle arrest in fission yeast associated with Rad24/14-3-3- dependent, Chkl/Cdsl-independent Weel upregulation [ J ] . Microbes Infect, 2006, 8:2736-2744.
  • 7Zheng F, He K, Li X, et al. Transient over-expression of TGFBR3 induces apoptosis in human nasopharyngeal carcinoma CNE-2Z cells[J]. Biosci Rep, 2013, e00029.
  • 8Rao JS. Molecular mechanisms of glioma invasiveness: the role of proteases [ J ]. Nat Rev Cancer, 2003,3:489 -501.
  • 9Du R, Petritsch C, Lu K, et al. Matrix metalloproteinase-2 reg- ulates vascular patterning and growth affecting tumor cell survival and invasion in GBM [ J ]. Neuro Oncol,2008 ,10 :254-264.
  • 10Page-McCaw A, Ewald A J, Werb Z. Matrix metalloproteinases and the regulation of tissue emodeling[ J]. Nat Rev Mol Cell Biol, 2007,8:221-233.

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