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首页> 外文期刊>Journal of cellular physiology. >Long noncoding RNA WDFY3-AS2 suppresses tumor progression by acting as a competing endogenous RNA of microRNA-18a in ovarian cancer
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Long noncoding RNA WDFY3-AS2 suppresses tumor progression by acting as a competing endogenous RNA of microRNA-18a in ovarian cancer

机译：长非编码RNA WDFY3-AS2抑制肿瘤作为竞争的内生发展RNA的microRNA-18a卵巢癌

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摘要

Ovarian cancer (OC) is a fatal cancer in women, mainly due to its aggressive nature and poor survival rate. The IncRNA-miRNA-mRNA (long noncoding RNA-microRNA-messenger RNA) interaction is promising biomarkers for the improving prognosis of OC. Therefore, we explored the regulatory mechanism of WDFY3-AS2/miR-18a/RORA axis involved in the biological activities of OC cells. Microarray analysis predicted differentially expressed IncRNA, miRNA, and mRNA related to OC, followed by investigating the relationship among them. The expression patterns of the identified IncRNA WDFY3-AS2, miR-18a, and RORA were measured in OC tissue and cells. Gain-and loss-of-function experiments were performed to characterize the effect of IncRNA WDFY3-AS2 on OC cells, as well as the involvement of miR-18a and RAR related orphan receptor A (RORA). The in vitro assays were validated by in vivo experiments. According to bioinformatics analysis, WDFY3-AS2 was speculated to affect OC by sponging miR-18a and modulating RORA. WDFY3-AS2 and RORA were underexpressed in OC, while miR-18a was highly expressed. Notably, WDFY3-AS2 acts as a competing endogenous RNA to sponge miR-18a and upregulate RORA. Upon overexpressing WDFY3-AS2 or inhibiting miR-18a, RORA expression was increased, thereby the OC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were suppressed, accompanied by enhanced apoptosis. In vivo experiments confirmed that the tumor growth was reduced in response to overexpressed WDFY3-AS2 or inhibited miR-18a. Taken together, the IncRNA WDFY3-AS2/miR-18a axis regulates the tumor progression of OC by targeting RORA, providing new insights for prevention and control of OC.
机译：卵巢癌女性(OC)是一种致命的癌症,主要是由于其激进的自然和贫穷存活率。非编码RNA RNA-microRNA-messenger)交互有前途的生物标志物是改善吗OC的预后。WDFY3-AS2 / miR-18a RORA基因的调控机制轴参与OC的生物活性细胞。差异表达IncRNA, microrna的mRNA有关OC,紧随其后的是调查它们之间的关系。识别IncRNA WDFY3-AS2 miR-18a,RORA基因测定在OC组织和细胞。增益和功能丧失实验用于描述IncRNA的效果WDFY3-AS2 OC细胞,以及参与miR-18a和RAR孤儿受体有关(RORA基因)。体内实验。分析,WDFY3-AS2猜测影响OC通过骗取miR-18a和调制RORA基因。WDFY3-AS2和RORA基因underexpressed OC,虽然miR-18a高度表达。WDFY3-AS2作为内源性RNA来竞争海绵miR-18a和上调RORA基因。overexpressing WDFY3-AS2或抑制miR-18a,RORA基因表达增加,从而OC细胞增殖、迁移、入侵和epithelial-to-mesenchymal过渡(EMT)镇压,伴随着增强细胞凋亡。体内实验证实了肿瘤的生长减少在回应中WDFY3-AS2或抑制miR-18a。的IncRNA WDFY3-AS2 / miR-18a轴调节针对RORA基因的肿瘤恶化的OC,为预防和控制提供了新的见解OC。

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