首页> 外文期刊>European review for medical and pharmacological sciences. >MNX1-AS1 accelerates the epithelial-mesenchymal transition in osteosarcoma cells by activating MNX1 as a functional oncogene
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MNX1-AS1 accelerates the epithelial-mesenchymal transition in osteosarcoma cells by activating MNX1 as a functional oncogene

机译:MNX1-AS1通过以官能团激活MNX1加速骨肉瘤细胞中的上皮 - 间充质转变

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OBJECTIVE: To investigate whether MNX1-AS1 can accelerate epithelial-mesenchymal transition (EMT) of osteosarcoma cells via activating MNX1. PATIENTS AND METHODS: The expression pattern of MNX1-AS1 in osteosarcoma tissues and cell lines was examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the cytoplasmic and nuclear levels of MNX1-AS1 in osteosarcoma cells were also determined. The regulatory effects of MNX1-AS1 on viability, clonality, migratory, and invasive abilities of the osteosarcoma cells were evaluated. The relative levels of MNX1 and EMT-related genes influenced by MNX1-AS1 were detected. The methylation ability in the promoter of the osteosarcoma cells transfected with si-MNX1-AS1 or MNX1-AS1 vector was determined by the whole genome bisulfite sequencing. RESULTS: MNX1-AS1 was upregulated in osteosarcoma tissues and cell lines, which was mainly expressed in the nucleus. The knockdown of MNX1-AS1 markedly attenuated viability, clonality, migratory, and the invasive abilities of the osteosarcoma cells. Besides, the transfection of si-MNX1-AS1 in U2OS and MG63 cells downregulated MNX1 and Snail, and upregulated E-cadherin. The methylation ability increased after the knockdown of MNX1-AS1, while the overexpression of MNX1-AS1 obtained the opposite trends. CONCLUSIONS: MNX1-AS1 mediates EMT of the osteosarcoma cells via activating MNX1, thereafter accelerating the progression of the osteosarcoma.
机译:目的:探讨MNX1-AS1是否可以通过活化MNX1加速骨肉瘤细胞的上皮 - 间充质转换(EMT)。患者和方法:通过定量实时 - 聚合酶链反应(QRT-PCR)检查骨肉瘤组织和细胞系中MNX1-AS1的表达模式。此外,还测定了骨肉瘤细胞中MNX1-AS1的细胞质和核水平。评估了MNX1-AS1对骨肉瘤细胞的活力,克隆,迁移和侵入能力的调节作用。检测到受MNX1-AS1影响的MNX1和EMT相关基因的相对水平。通过全基因组亚硫酸氢盐测序测定转染与Si-MNX1-AS1或MNX1-AS1载体转染的骨肉瘤细胞启动子的甲基化能力。结果:MNX1-AS1上调在骨肉瘤组织和细胞系中,主要在细胞核中表达。 MNX1-AS1的敲低明显减弱了骨肉瘤细胞的可活力,克隆性,迁移和侵入能力。此外,U2OS和Mg63细胞中的Si-Mnx1-AS1的转染下调MNX1和蜗牛,并上调的E-Cadherin。甲基化能力在MNX1-AS1的敲低后增加,而MNX1-AS1的过表达获得相反的趋势。结论:MNX1-AS1通过激活MNX1介导骨肉瘤细胞的EMT,之后加速骨肉瘤的进展。

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