Suppr超能文献

EphA1 受体通过小干扰 RNA 沉默具有抗血管生成和抗肿瘤功效在肝细胞癌。

EphA1 receptor silencing by small interfering RNA has antiangiogenic and antitumor efficacy in hepatocellular carcinoma.

机构信息

Department of Hepatobiliary Surgery, The First Affiliated Hospital, Wenzhou Medical College, Wenzhou, PR China.

出版信息

Oncol Rep. 2010 Feb;23(2):563-70.

Abstract

The Eph family of receptor tyrosine kinases has emerged as one of the pivotal regulators of tumor angiogenesis. EphA1, the first identified member of the Eph receptor family, has been found to be overexpressed in several types of human tumors. A recent report indicated that EphA1 was overexpressed in hepatocellular carcinoma (HCC) and that elevated expression of EphA1 can promote proliferation of HCC cells through stimulation by exogenous Ephrin-A1. To investigate the role of EphA1 in angiogenesis and progression of HCC, we down-regulated EphA1 by RNA interference (RNAi) technology, in an HCC-derived cell line with a high level of EphA1 expression. We established a stable knockdown clone named SiEphA1/Huh-7. The knockdown resulted in decreased proliferation of Huh-7 cells, as well as decreased motility and invasion capability in vitro. siRNA-based EphA1 knockdown also down-regulated the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-2 and -9. Interestingly, the suppression of EphA1 expression in Huh-7 cells reduced their outgrowth when inoculated in the subcutaneous space in the flank of nude mice, presumably through angiogenesis inhibition since microvessel density was found to be inhibited.

摘要

Eph 家族的受体酪氨酸激酶已成为肿瘤血管生成的关键调节因子之一。EphA1 是 Eph 受体家族中第一个被鉴定的成员,已发现在多种类型的人类肿瘤中过度表达。最近的一份报告表明 EphA1 在肝细胞癌 (HCC) 中过度表达,EphA1 的高表达可以通过外源性 Ephrin-A1 的刺激促进 HCC 细胞的增殖。为了研究 EphA1 在 HCC 血管生成和进展中的作用,我们通过 RNA 干扰 (RNAi) 技术下调 EphA1 在 EphA1 表达水平较高的 HCC 细胞系中。我们建立了一个稳定的敲低克隆,命名为 SiEphA1/Huh-7。敲低导致 Huh-7 细胞增殖减少,体外迁移和侵袭能力降低。基于 siRNA 的 EphA1 敲低还下调了血管内皮生长因子 (VEGF) 和基质金属蛋白酶 (MMP)-2 和 -9 的表达。有趣的是,在裸鼠的侧腹皮下空间接种时,Huh-7 细胞中 EphA1 表达的抑制减少了它们的生长,推测是通过抑制血管生成,因为发现微血管密度受到抑制。

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