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首页> 外文期刊>Cellular Physiology and Biochemistry >Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195
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Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

机译:lncRNA UCA1沉默通过miR-195抑制人微血管内皮细胞的生长和管形成

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Background/Aims Recent studies have suggested that several lncRNAs contribute to the angiogenic function of endothelial cells. Herein, we set out to reveal whether lncRNA UCA1 has functions in endothelial angiogenesis. Methods The expression levels of lncRNA UCA1, miR-195 and CCND1 in human microvascular endothelial HMEC-1 cells were altered by transfection. Subsequently, cell viability, migration, tube formation and apoptosis of HMEC-1 cells were respectively assessed. The cross-talk between lncRNA UCA1, miR-195, CCND1, and MEK/ERK and mTOR signaling pathways were investigated by performing qRT-PCR and Western blotting. Results Silence of lncRNA UCA1 repressed HMEC-1 cells viability, migration, tube formation, and induced apoptosis. Meanwhile, silence of lncRNA UCA1 significantly up-regulated miR-195 expression. These alterations induced by lncRNA UCA1 were further enhanced by miR-195 overexpression, while were attenuated by miR-195 suppression. Moreover, silence of lncRNA UCA1 deactivated MEK/ERK and mTOR signaling pathways via a miR-195-dependent regulation. And the deactivation of MEK/ERK and mTOR signaling pathways led to a down-regulation of CCND1. Conclusion This study demonstrates that silence of lncRNA UCA1 largely represses microvascular endothelial cells growth and tube formation. Silence of lncRNA UCA1 exerts its function possibly via up-regulation of miR-195, which in turn inactivates MEK/ERK and mTOR signaling pathways, and ultimately represses CCND1 expression.
机译:背景/目的最近的研究表明,几种lncRNA有助于内皮细胞的血管生成功能。在这里,我们着手揭示lncRNA UCA1是否在内皮血管生成中具有功能。方法通过转染改变人微血管内皮HMEC-1细胞中lncRNA UCA1,miR-195和CCND1的表达水平。随后,分别评估了HMEC-1细胞的细胞活力,迁移,管形成和凋亡。通过执行qRT-PCR和Western印迹研究了lncRNA UCA1,miR-195,CCND1和MEK / ERK与mTOR信号通路之间的串扰。结果lncRNA UCA1沉默可抑制HMEC-1细胞的活力,迁移,管形成并诱导凋亡。同时,lncRNA UCA1的沉默显着上调了miR-195的表达。由lncRNA UCA1诱导的这些改变通过miR-195过表达进一步增强,而通过miR-195抑制而减弱。此外,lncRNA UCA1的沉默通过miR-195依赖性调控使MEK / ERK和mTOR信号通路失活。 MEK / ERK和mTOR信号通路的失活导致CCND1的下调。结论这项研究表明,lncRNA UCA1的沉默在很大程度上抑制了微血管内皮细胞的生长和管的形成。 lncRNA UCA1沉默可能通过上调miR-195发挥其功能,进而上调MEK / ERK和mTOR信号通路,并最终抑制CCND1表达。

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