Suppr超能文献

微小RNA-93在血管生成调节中的作用。

Role of microRNA-93 in regulation of angiogenesis.

作者信息

Li Fangxuan, Liang Xiaofeng, Chen Ying, Li Shixia, Liu Juntian

机构信息

Department of Cancer Prevention Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.

出版信息

Tumour Biol. 2014 Nov;35(11):10609-13. doi: 10.1007/s13277-014-2605-6. Epub 2014 Sep 14.

Abstract

Angiogenesis is essential for a wide variety of physiological and pathological processes. To date, many angiogenic microRNAs (miRNAs) have been identified and several of them were further investigated to elucidate the mechanisms of specific miRNAs in regulating angiogenesis. In recent studies concerning tumor and ischemia, the miRNA-93 had been demonstrated to be able to modulate angiogenesis in different molecular pathways. The miRNA-93 can promote angiogenesis via enhancing endothelial cell proliferation, migration, and tube formation. Additionally, miRNA-93-over-expressing cells developed a relationship with the blood vessels allowing tumor cells to survive and to grow well. However, high expression of miRNA-93 can depress the vascular endothelial growth factor (VEGF) secretion and its downstream molecular targets in in vivo and vitro experiments. MiRNA-93's effects on angiogenesis are dependent on the interaction of other multiple genes and signal pathways, such as P21, E2F1, integrin-β8, LATS2, etc. Future investigation should involve mapping the network by which miRNA-93 exerts its functions.

摘要

血管生成对于多种生理和病理过程至关重要。迄今为止,许多血管生成性微小RNA(miRNA)已被鉴定出来,其中一些还被进一步研究以阐明特定miRNA在调节血管生成中的机制。在最近关于肿瘤和缺血的研究中,miRNA - 93已被证明能够在不同的分子途径中调节血管生成。miRNA - 93可通过增强内皮细胞增殖、迁移和管腔形成来促进血管生成。此外,过表达miRNA - 93的细胞与血管建立了联系,使肿瘤细胞得以存活并良好生长。然而,在体内和体外实验中,miRNA - 93的高表达可抑制血管内皮生长因子(VEGF)的分泌及其下游分子靶点。miRNA - 93对血管生成的影响取决于其他多个基因和信号通路的相互作用,如P21、E2F1、整合素 - β8、LATS2等。未来的研究应涉及绘制miRNA - 93发挥其功能的网络图谱。

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