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首页> 外文期刊>European review for medical and pharmacological sciences. >Knockdown of long noncoding RNA DLX6-AS1 inhibits cell proliferation and invasion of cervical cancer cells by downregulating FUS
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Knockdown of long noncoding RNA DLX6-AS1 inhibits cell proliferation and invasion of cervical cancer cells by downregulating FUS

机译:长度非编码RNA DLX6-AS1的敲低通过下调FU来抑制细胞增殖和宫颈癌细胞的侵袭

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摘要

OBJECTIVE: Recently, the vital role of long noncoding RNAs (lncRNAs) in human diseases have got much attention. In this research, lncRNA DLX6-AS1 is studied to verify how it affects the development of cervical cancer (CC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in both CC cells and tissue samples. Besides, functional experiments including cell counting kit-8 (CCK-8) assay, colony formation assay, and transwell assay were performed. Meanwhile, the underlying mechanism was explored through qRT-PCR and Western blot assay. The function of DLX6-AS1 was also identified in vivo. RESULTS: By comparing with corresponding tissues, the DLX6-AS1 expression level was significantly higher in CC samples. Moreover, cell growth ability and invaded ability of CC cells were inhibited after DLX6-AS1 was knocked down. Furthermore, the expression of FUS was inhibited after knockdown of DLX6-AS1. It was found that the expression level of FUS positively correlated to the expression of DLX6-AS1 in CC tissues. In addition, knockdown of DLX6-AS1 inhibited tumor formation and metastasis of CC in nude mice. CONCLUSIONS: These results suggest that DLX6-AS1 could enhance cell proliferation and metastasis of CC by upregulating FUS, which might be a potential therapeutic target in CC.
机译:目的:最近,长期非编码RNA(LNCRNA)在人类疾病中的重要作用得到了很大的关注。在本研究中,研究了LNCRNA DLX6-AS1,以验证它如何影响宫颈癌的发育(CC)。患者和方法:在CC细胞和组织样品中通过定量实时 - 聚合酶链反应(QRT-PCR)检测DLX6-AS1表达。此外,进行包括细胞计数试剂盒-8(CCK-8)测定,菌落形成测定和Transwell测定的功能实验。同时,通过QRT-PCR和Western印迹测定探索潜在机制。 DLX6-AS1的功能也在体内鉴定。结果:通过与相应组织进行比较,CC样品中DLX6-AS1表达水平显着高。此外,在将DLX6-AS1撞击后抑制CC细胞的细胞生长能力和侵袭能力。此外,在DLX6-AS1的敲尾后抑制FUS的表达。发现Fus的表达水平与CC组织中DLX6-AS1的表达呈正相关。此外,DLX6-AS1的敲低抑制裸鼠中CC的肿瘤形成和转移。结论:这些结果表明DLX6-AS1可以通过上调FU来增强CC的细胞增殖和转移,这可能是CC中的潜在治疗靶标。

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