首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Long non-coding RNA FAM99A modulated YAP1 to affect trophoblast cell behaviors in preeclampsia by sponging miR-134-5p
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Long non-coding RNA FAM99A modulated YAP1 to affect trophoblast cell behaviors in preeclampsia by sponging miR-134-5p

机译:长期非编码RNA FAM99A调制YAP1通过冲水MIR-134-5P影响预液位血管蛋白的滋养细胞行为

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摘要

Preeclampsia (PE) is a complex pregnancy syndrome. Convincing evidence indicates that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of PE. This research mainly investigated the mechanism of family with sequence similarity 99 member A (FAM99A) in PE. The expressions of FAM99A, miR-134-5p, and YAP1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell apoptosis, migration, and invasion were detected by flow cytometry or transwell assay. The interaction between miR-134-5p and FAM99A or YAP1 was confirmed by dual-luciferase reporter assay. The protein expression of YAP1 was determined by western blot assay. FAM99A and YAP1 were significantly up-regulated, and miR-134-5p was significantly down-regulated in PE tissues (n=30). miR-134-5p was verified as a candidate of FAM99A and YAP1. FAM99A promoted cell metastasis, but reduced apoptosis in HTR8/SVneo cells by regulating miR-134-5p. miR-134-5p down-regulated YAP1 expression to suppress cell metastasis, while it induced apoptosis in HTR8/SVneo cells. FAM99A positively modulated YAP1 expression by sponging miR-134-5p. FAM99A modulated YAP1 to accelerate cell migration and invasion, and inhibited cell apoptosis in PE cells by sponging miR-134-5p. The novel regulatory network may shed light on the pathogenesis of PE.
机译:Preclampsia(PE)是一种复杂的妊娠综合征。令人信服的证据表明,长期非编码RNA(LNCRNA)参与PE的发病机制。本研究主要研究了PE中序列相似性99成员A(FAM99A)的家庭机制。通过定量的实时聚合酶链反应(QRT-PCR)检测FAM99A,MIR-134-5P和YAP1的表达。通过流式细胞术或Transwell测定检测细胞凋亡,迁移和侵袭。通过双荧光素酶报告器测定证实了MiR-134-5P和FAM99A或YAP1之间的相互作用。通过蛋白质印迹测定法测定YAP1的蛋白质表达。 FAM99A和YAP1显着上调,MIR-134-5P在体育组织中显着下调(n = 30)。 MIR-134-5P被验证为FAM99A和YAP1的候选人。 FAM99A促进细胞转移,但通过调节miR-134-5p,在HTR8 / SVNEO细胞中降低了细胞凋亡。 miR-134-5p下调的yap1表达,以抑制细胞转移,而在Htr8 / svneo细胞中诱导细胞凋亡。 FAM99A通过海绵MIR-134-5P正呈粘性YAP1表达。 FAM99A调制YAP1加速细胞迁移和侵袭,并通过冲水-134-5p抑制PE细胞中的细胞凋亡。新型调节网络可能揭示PE的发病机制。

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