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首页> 外文期刊>Journal of cellular and molecular medicine. >LncRNA SNHG1 functions as a ceRNA to antagonize the effect of miR‐145a‐5p on the down‐regulation of NUAK1 in nasopharyngeal carcinoma cell
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LncRNA SNHG1 functions as a ceRNA to antagonize the effect of miR‐145a‐5p on the down‐regulation of NUAK1 in nasopharyngeal carcinoma cell

机译:LncRNA SNHG1作为ceRNA来拮抗miR‐145a‐5p对鼻咽癌细胞NUAK1下调的影响

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How lncRNA SNHG1 influences the aggressiveness of nasopharyngeal carcinoma cells as well as the underlying mechanism was studied. The lncRNA differences were analysed by GSE12452 gene microarray. The expression of SNHG1, MiR‐145‐5p and NUAK1 was identified by qRT‐PCR and western blot. Transfection was conducted to construct nasopharyngeal carcinoma cells with different expressions of SNHG1, miR‐145‐5p and NUAK1 . Dual‐luciferase reporter assay was performed to explore the relationship between SNHG1, miR‐145‐5p and NUAK1 . Wound‐healing assay and transwell invasion experiments were employed to study changes in cell migration capacity and cell invasion, respectively. Tumour xenografts were performed to observe lung metastasis of nude mice inoculated with transfected CNE cells. SNHG1 is highly expressed in nasopharyngeal carcinoma tissues and in cell lines. Down‐regulation of SNHG1 facilitated the expression of miR‐145‐5p and further suppressed the level of NAUK1 in CNE and HNE‐1 cells. Silencing of SNHG1, up‐regulation of miR‐145‐5p and inhibition of NAUK1 by relative transfection all attenuated the aggressiveness of CNE and HNE‐1 cells both in vivo and in vitro . Moreover, the impaired cell migration and invasion by SNHG1 siRNA could be rescued by cotransfection of miR‐145‐5p in CNE and HNE‐1 cells. LncRNA SNHG1 promoted the expression of NUAK1 by down‐regulating miR‐145‐5p and thus promoted the aggressiveness of nasopharyngeal carcinoma cells through AKT signalling pathway and induced epithelial‐mesenchymal transition (EMT).
机译:研究了lncRNA SNHG1如何影响鼻咽癌细胞的侵袭性及其潜在机制。通过GSE12452基因微阵列分析lncRNA差异。通过qRT-PCR和Western blot鉴定了SNHG1,MiR145-5p和NUAK1的表达。进行转染以构建具有不同SNHG1,miR‐145-5p和NUAK1表达的鼻咽癌细胞。进行了双重荧光素酶报告基因检测,以探讨SNHG1,miR‐145-5p和NUAK1之间的关系。伤口愈合试验和穿孔侵袭实验分别用于研究细胞迁移能力和细胞侵袭的变化。进行肿瘤异种移植以观察接种了转染的CNE细胞的裸鼠的肺转移。 SNHG1在鼻咽癌组织和细胞系中高表达。 SNHG1的下调促进了miR-1145-5p的表达,并进一步抑制了CNE和HNE-1细胞中NAUK1的水平。 SNHG1的沉默,miR‐145-5p的上调和相对转染对NAUK1的抑制均减弱了CNE和HNE-1细胞在体内和体外的侵袭性。此外,通过在CNE和HNE-1细胞中共转染miR‐145-5p,可以挽救SNHG1 siRNA受损的细胞迁移和侵袭。 LncRNA SNHG1通过下调miR-145-5p来促进NUAK1的表达,从而通过AKT信号通路促进鼻咽癌细胞的侵袭性并诱导上皮-间质转化(EMT)。

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