血管内皮生长因子(VEGF):基因调控模型和肿瘤侵袭性标志物。一个明显的治疗目标?

Journal de la Societe de biologie Pub Date : 2009-01-01 Epub Date: 2009-06-16 DOI:10.1051/jbio/2009022
Renaud Grépin, Gilles Pagès
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引用次数: 4

摘要

VEGF是一种基因表达调控模型。RAS/RAF/MEK/ERK和PI3激酶通路被生长因子刺激或癌基因激活,通过激活转录因子或灭活与mRNA降解有关的蛋白来促进其表达。这些因子(Sp1/Sp3, HIF-1和TTP)构成肿瘤侵袭性的分子标记。VEGF在实体瘤或血液肿瘤中过表达。因此,许多以VEGF为靶点调节血管生成的化合物已经被开发出来。然而,它们的效果并不像预期的那么壮观。VEGF的抗血管生成异构体的存在可能是其活性较弱的原因。本文将讨论这些不同的观点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The vascular endothelial growth factor (VEGF): a model of gene regulation and a marker of tumour aggressiveness. An obvious therapeutic target?].

VEGF represents a model of gene expression regulation. RAS/RAF/MEK/ERK and PI3 Kinase pathways, activated in response to growth factors stimulation or by oncogenes, contribute to its expression by activating transcription factors or inactivating proteins implicated in degradation of its mRNA. These factors (Sp1/Sp3, HIF-1 and TTP) constitute molecular markers of tumor aggressiveness. VEGF is overexpressed in solid or hematologic tumors. Thus, numerous compounds regulating angiogenesis by targeting VEGF have been developed. However, their effects are not as spectacular as expected. The existence of anti-angiogenic isoforms of VEGF could be a cause of their less potent activity. These different points are discussed in this review article.

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