Tenascin-C protein is induced by Transforming Growth Factor-β1 but does not correlate with time to tumor progression in high-grade gliomas
Tenascin-C protein is induced by Transforming Growth Factor-β1 but does not correlate with time to tumor progression in high-grade gliomas
复制标题
DOI：
10.1007/s11060-005-9000-5
复制
发表时间：
2006-03-01
影响因子：
3.9
通讯作者：
Bosserhoff, AK
中科院分区：
文献类型：
--
作者：
Hau, P;Kunz-Schughart, LA;Bosserhoff, AK
背景资料：生腱蛋白-C是已知与胶质母细胞瘤患者的预后相关的细胞外基质蛋白，可能通过刺激侵袭和新血管生成。转化生长因子-β 1（TGF-β 1）在高级别胶质瘤的生物学中起重要作用，部分通过调节这些肿瘤向实质的侵袭。本研究的目的是评估如果TGF-β 1诱导的表达和沉积的Tenascin-C的细胞外基质中的高级别胶质瘤，这可能是关键的这些肿瘤的侵袭到健康parenchyma.Methods：一系列的20个高级别胶质瘤进行染色，Tenascin-C-和TGF-β 1-特异性抗体。两种蛋白质的表达水平进行了评估，并相互关联，进展时间和分子和形态学标志物的侵袭。定量PCR分析进行评估的诱导Tenascin-C mRNA的治疗与TGF-β 1 in vitro.Results：Tenascin-C表达在18的19（95%）可评估的肿瘤，而14的20个肿瘤（70%）表达TGF-β 1的细胞的显着百分比。TGF-β 1在体外诱导Tenascin-C在mRNA和蛋白水平的表达。Tenascin-C和TGF-β 1的表达相互之间没有统计学相关性，也与进展时间无关。结论：在我们的系列中，Tenascin-C和TGF-β 1在绝大多数高级别胶质瘤中表达。我们无法检测到其中一种蛋白质与进展时间的相关性。然而，我们描述了TGF-β 1诱导生腱蛋白-C，这可能为高级别胶质瘤向健康实质的侵袭提供了机制。
Background: Tenascin-C is an extracellular matrix protein known to correlate with prognosis in patients with glioblastoma, probably by stimulation of invasion and neoangiogenesis. Transforming Growth Factor-beta 1 (TGF-beta 1) plays an important role in the biology of high-grade gliomas, partly by regulating Invasion of these tumors into parenchyma. This study was designed to evaluate if TGF-beta 1 induces the expression and deposition of Tenascin-C in the extracellular matrix of high-grade gliomas which may be pivotal for the invasion of these tumors into healthy parenchyma.Methods: A series of 20 high-grade gliomas was stained immunohistochemically with Tenascin-C- and TGF-beta 1-specific antibodies. Expression levels of both proteins were evaluated and correlated with each other, time to progression and molecular and morphological markers of invasion. A quantitative PCR assay was performed evaluating the induction of Tenascin-C mRNA by treatment with TGF-beta 1 in vitro.Results: Tenascin-C was expressed in 18 of 19 (95%) evaluable tumors, whereas 14 of 20 tumors (70%) expressed TGF-beta 1 in a significant percentage of cells. Treatment with TGF-beta 1 did induce the expression of Tenascin-C at the mRNA and protein level in vitro. The expression of Tenascin-C and TGF-beta 1 did neighter statistically correlate with each other nor with time to progression.Conclusion: In our series, Tenascin-C and TGF-beta 1 were expressed in the vast majority of high-grade gliomas. We could not detect a correlation of one of the proteins with time to progression. Nevertheless, we describe induction of Tenascin-C by TGF-beta 1, possibly providing a mechanism for the invasion of high-grade gliomas into healthy parenchyma.