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LncRNA FLVCR1-AS1 mediates miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in ovarian cancer

机译:LNCRNA FLVCR1-AS1介导MIR-513 / YAP1信号传导,以促进卵巢癌中的细胞进展,迁移,入侵和EMT过程

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摘要

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with the proliferation of several cancer cells. The aim of this study was to investigate the role of FLVCR1-AS1 in ovarian serous cancer (OSC). Methods FLVCR1-AS1 expression was determined in human OSC tissues, serums and cell lines. The role of FLVCR1-AS1 knockdown or overexpression on OSC cell growth, migration, invasion, apoptosis and epithelial to mesenchymal transition (EMT) were evaluated in vitro using CCK8, colony formation assay, wound healing assay, transwell assay and western blot assay. Besides, luciferase reporter assays were performed to identify interactions among FLVCR1-AS1 and its target genes. Moreover, the in vivo effects were investigated using immunocompromised NSG female mice. Results In this study, FLVCR1-AS1 expression was upregulated in OSC tissues, serums, and cells. Knockdown FLVCR1-AS1 decreased cell growth, migration, invasion, and EMT, as well as increased apoptosis in OSC cells, whereas, overexpression of FLVCR1-AS1 increased cell proliferation, migration, invasion, and EMT, and decreased apoptosis of OSC cells. Besides, FLVCR1-AS1 directly bound to miR-513 and downregulated its expression. Moreover, FLVCR1-AS1 reversed the effect of miR-513 on the OSC cell growth, which might be associated with the role of YAP1. Furthermore, in terms of mechanism, FLVCR1-AS1 promoted EMT in OSC cells. Finally, mice models further confirmed that knockdown FLVCR1-AS1 distinctly suppressed cell growth and EMT in vivo. Conclusion Taken together, FLVCR1-AS1 mediated miR-513/YAP1 signaling to promote cell progression, migration, invasion and EMT process in OSC cells.
机译:据报道,据报道,据报道,据报道,长的非分量RNA(LNCRNA)与几种癌细胞的增殖相关。本研究的目的是探讨FLVCR1-AS1在卵巢浆液癌(OSC)中的作用。方法在人OSC组织,血清和细胞系中测定FLVCR1-AS1表达。使用CCK8,菌落形成测定,伤口愈合测定,Transwell测定和Western印迹测定,在体外评估FLVCR1-AS1敲低或过度表达对osc细胞生长,迁移,侵袭,凋亡和上皮进行间充质转换(EMT)的作用。此外,进行荧光素酶报告器测定以鉴定FLVCR1-AS1及其靶基因之间的相互作用。此外,使用免疫调节NSG雌性小鼠研究了体内效应。结果在该研究中,在OSC组织,血清和细胞中升高了FLVCR1-AS1表达。敲低FLVCR1-AS1降低细胞生长,迁移,侵袭和EMT,以及血晶细胞中的细胞凋亡增加,而FLVCR1-AS1的过度表达增加了细胞增殖,迁移,侵袭和EMT,并降低了OSC细胞的凋亡。此外,FLVCR1-AS1直接绑定到MIR-513并下调其表达。此外,FLVCR1-AS1逆转MIR-513对OSC细胞生长的影响,这可能与YAP1的作用相关。此外,在机制方面,FLVCR1-AS1在OSC细胞中促进EMT。最后,小鼠模型进一步证实,敲低FLVCR1-AS1明显抑制细胞生长和体内EMT。结论,FLVCR1-AS1介导的MIR-513 / YAP1信号传导,以促进OSC细胞中的细胞进展,迁移,侵袭和EMT过程。

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