Suppr超能文献

2-苯甲酰基苯氧基乙酰胺对艾氏腹水瘤细胞的抗血管生成作用是由缺氧诱导因子-1α介导的,并在体内下调血管内皮生长因子。

Antiangiogenic effect of 2-benzoyl-phenoxy acetamide in EAT cell is mediated by HIF-1alpha and down regulation of VEGF of in-vivo.

作者信息

Prabhakar B T, Khanum Shaukath Ara, Shashikanth S, Salimath Bharathi P

机构信息

Department of Studies in Applied Botany & Biotechnology, University of Mysore, Manasagangotri, Mysore 570006, India.

出版信息

Invest New Drugs. 2006 Nov;24(6):471-8. doi: 10.1007/s10637-006-6587-0.

Abstract

Benzophenones and its analogues are known for wide range of biological properties. Synthetic benzophenone analogue 2-benzoyl -phenoxy acetamide (BP-1) is proven to be potent antitumor and proapoptotic activity against EAT cells in-vivo. In the present report, we studied the antiangiogenic effect of BP-1 in EAT cells induced angiogenesis. Treatment with BP-1 in-vivo was demonstrated by the down regulation of the secretion of VEGF from EAT cells and inhibition of blood vessels formation indicating the potential angioinhibitory effect of BP-1 in EAT cells. HIF-1alpha protein, a transcription factor known to be key a regulator in hypoxia-induced angiogenesis was also down regulated by BP-1. Our findings indicated that, HIF-1alpha nuclear sequestration is repressed by BP-1 through inhibition of nuclear translocation. We postulate that diminished HIF-1alpha nuclear presence and activity in BP-1 treated EAT cells could be responsible for decreased VEGF expression and antiangiogenic effects.

摘要

二苯甲酮及其类似物因其广泛的生物学特性而闻名。合成二苯甲酮类似物2-苯甲酰基-苯氧基乙酰胺(BP-1)在体内对艾氏腹水瘤(EAT)细胞具有强大的抗肿瘤和促凋亡活性。在本报告中,我们研究了BP-1对EAT细胞诱导的血管生成的抗血管生成作用。体内用BP-1处理表现为EAT细胞VEGF分泌下调以及血管形成受到抑制,这表明BP-1在EAT细胞中具有潜在的血管生成抑制作用。HIF-1α蛋白是一种已知在缺氧诱导的血管生成中起关键调节作用的转录因子,它也被BP-1下调。我们的研究结果表明,BP-1通过抑制核转位来抑制HIF-1α的核隔离。我们推测,在BP-1处理的EAT细胞中,HIF-1α核内存在和活性的降低可能是VEGF表达下降和抗血管生成作用的原因。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验