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E2EPF Ubiquitin Carrier Protein-Von Hippel-Lindau Interaction and Uses Thereof

机译:E2EPF泛素载体蛋白-冯Hippel-林道相互作用及其用途

摘要

The present invention relates to the E2EPF UCP-VHL interaction and the uses thereof, more precisely a method for increasing or reducing VHL activity or level by regulating UCP activity or level to inhibit cancer cell proliferation or metastasis or to increase angiogenesis. The inhibition of UCP activity is accomplished by any UCP activity inhibitor selected from a group consisting of a small interfering RNA (RNAi), an antisense oligonucleotide, and a polynucleotide complementarily binding to mRNA of UCP, a peptide, a peptide mimetics and an antibody, and a low molecular compound. In the meantime, the increase of angiogenesis is accomplished by the following mechanism; UCP over-expression is induced by a gene carrier and thus endogenous VHL is reduced, leading to the stabilization of HIF-1α which enhances VEGF activation based on the HIF-1α stabilization. The method for regulating UCP activity or level results in the increase or decrease of VHL activity or level, so that it can be applied to the development of an anticancer agent and an angiogenesis inducer.
机译:本发明涉及E2 EPF VHL相互作用及其用途,更准确地说,涉及通过调节UCP活性或水平来抑制或抑制癌细胞的增殖或转移而增加或降低VHL活性或水平的方法。增加血管生成。可以通过选自小干扰RNA(RNAi),反义寡核苷酸和与UCP mRNA,肽,肽模拟物和抗体互补结合的多核苷酸的任何UCP活性抑制剂来实现对UCP活性的抑制。和低分子化合物。同时,血管生成的增加是通过以下机制完成的: UCP过表达由基因载体诱导,因此内源性VHL降低,从而导致HIF-1α稳定,从而基于HIF-1α的稳定性增强VEGF的激活。调节UCP活性或水平的方法导致VHL活性或水平的增加或降低,因此其可用于开发抗癌剂和血管生成诱导剂。

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