[血管生成与肿瘤侵袭的相似性]。

D Stéhelin
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引用次数: 0

摘要

我们已经证明,给定的细胞因子能够在两种非常不同的细胞类型中诱导Ets家族转录因子的表达:1)血管内皮细胞,但仅在新生血管形成期间;2)肿瘤周围基质的纤维细胞,但仅当这些肿瘤具有侵袭性特征时。在这种情况下,纤维细胞也表达一些金属蛋白酶(胶原酶1,尿激酶纤溶酶原激活剂,有时也表达基质溶酶1)。在离体重建实验中,我们证明了相应的基因被Ets家族转录因子直接上调,通常与转录复合体Jun/Fos相关。这种蛋白酶被认为能破坏基质,使侵袭性肿瘤进一步扩大。我们推测,Ets因子的失活可能严重阻碍新生血管的形成和肿瘤的扩张。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Similarities between angiogenesis and neoplasm invasiveness ].

We have shown that given cytokines are capable of inducing the expression of transcription factors of the Ets family in two very distinct cell types: 1) endothelial cells of blood vessels, but only during neovascularization, and 2) fibrocytic cells from stroma surrounding tumors, but only if these tumors bear characteristics of invasiveness. In such cases, the fibrocytic cells also express some metalloproteinases (collagenase 1, urkinase plasminogen activator, sometimes stromelysin1). In ex vivo reconstruction experiments, we demonstrate that the corresponding genes are directly up-regulated by the Ets family transcription factors, often associated with the transcription complex Jun/Fos. The proteinases are thought to dismantle the stroma and allow invasive tumors to proceed toward further expansion. We speculate that inactivation of the Ets factors could seriously hamper both neovascularization and tumor expansion.

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