The long noncoding RNA uc.294 is upregulated in early-onset pre-eclampsia and inhibits proliferation, invasion of trophoblast cells (HTR-8/SVneo)

The long noncoding RNA uc.294 is upregulated in early-onset pre-eclampsia and inhibits proliferation, invasion of trophoblast cells (HTR-8/SVneo)
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长非编码 RNA uc.294 在早发性先兆子痫中表达上调,并抑制滋养层细胞的增殖和侵袭 (HTR-8/SVneo)

DOI:
10.1002/jcp.27916
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发表时间:
2019-07-01
影响因子:
5.6
通讯作者:
Long, Wei
Long, Wei
中科院分区:
生物学2区
文献类型:
--
作者:
Song, Xuejing;Li, Chunyan;Long, Wei

文献摘要

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近年来,大量长链非编码rna (lncRNAs)在人类疾病中被报道为进化保守的,可能在包括先兆子痫在内的许多生物学事件中发挥作用。在我们之前的研究中,我们选择了数千个lncrna来研究它们与早发性先兆子痫的关系。在这些lncRNA中,一种名为uc的lncRNA。294引起了我们的注意,曾有报道在早发性子痫前期特异性高水平表达。本研究旨在探讨uc的功能。294例早发性先兆子痫及其可能的机制加州大学。采用实时定量聚合酶链反应(pcr)检测294在早发型子痫前期和正常胎盘组织中的表达水平。为了检测滋养层细胞的增殖、侵袭和凋亡能力,我们分别进行了细胞计数试剂盒-8实验、transwell实验和流式细胞术。在这里,我们首次报道,uc。294通过作用于滋养细胞HTR-8/SVneo的关键生物学行为抑制增殖、侵袭和促进凋亡。然而,如何uc。294在早发型先兆子痫中调控基因功能的作用有待进一步探讨。
Recently, a large number of long noncoding RNAs (lncRNAs) have been reported in human diseases that are evolutionarily conserved and are likely to play a role in many biological events including pre-eclampsia. In our previous research, we selected thousands of lncRNAs for their relationship with early-onset pre-eclampsia. Among these lncRNAs, a lncRNA named uc.294 attracted our attention, was once reported to specifically be expressed at a high level in the early-onset of pre-eclampsia. This study aims to investigate the function of uc.294 in early-onset pre-eclampsia and the possible mechanism. The uc.294 expression level in early-onset pre-eclampsia or in normal placenta tissues was evaluated by quantitative real-time polymerase chain reaction. To detect the proliferation, invasion, and apoptosis capacity of the trophoblast cells, we performed the Cell Counting Kit-8 assay, transwell assay, and flow cytometry, respectively. Here we report, for the first time, that uc.294 inhibits proliferation, invasion, and promotes apoptosis of trophoblast cells HTR-8/SVneo by working in key aspects of biological behaviors. However, how uc.294 acts to regulate gene functions in early-onset pre-eclampsia needs further exploration.