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首页> 外文期刊>European review for medical and pharmacological sciences. >Long-chain non-coding RNA Linc00888 promotes the proliferation and migration of esophageal cancer cells by downregulating miR-34a expression
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Long-chain non-coding RNA Linc00888 promotes the proliferation and migration of esophageal cancer cells by downregulating miR-34a expression

机译:长链非编码RNA LINC00888通过下调miR-34a表达来促进食管癌细胞的增殖和迁移

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摘要

OBJECTIVE: To explore the role and potential mechanism of long-chain non-coding RNA 00888 in esophageal cancer (EC). PATIENTS AND METHODS: The expression level of Linc00888 in esophageal cancer tissues and adjacent ones, as well as corresponding cell lines, was measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Survival prognosis information of patients was collected, and KM survival analysis was performed to determine the prognostic value of Linc00888. To better understand the effect of Linc00888 on the proliferative and migration ability of EC cells, Cell Counting Kit-8 (CCK-8), clone formation, and transwell assays were performed after Linc00888 was knocked down in EC cell lines. Furthermore, bioinformatics prediction website was used to discover the potential target of Linc00888. Then, Dual-Luciferase reporter gene assay was performed to verify the binding relationship between Linc00888 and the downstream gene miR-34a. Then, the expression relationship between the two was measured both in cell lines and tissues. Finally, to clarify the regulation between Linc00888 and miR-34a, a recovery experiment was performed using co-transfection technology. RESULTS: Linc00888 was aberrantly upregulated in esophageal cancer tissues. The survival analysis showed that the higher expression of Linc00888 was significantly correlated with shorter overall survival. Cell functional experiment results suggested that Linc00888 played a role in promoting tumor proliferative and migration ability in EC cells. Besides, Dual-Luciferase reporter genes assay indicated that miR-34a and Linc00888 had binding sites. Meanwhile, we confirmed that there was a negative correlation between the expression levels of miR-34a and Linc00888 in cells and tissues. Cellular functional recovery experiments revealed that Linc00888 could modulate the progression of EC by miR-34a. CONCLUSIONS: Linc00888 promotes the proliferative and migration ability of EC through miR-34a.
机译:目的:探讨长链非编码RNA 00888在食管癌(EC)中的作用和潜在机制。患者和方法:通过定量实时聚合酶链反应(QRT-PCR)测量食管癌组织和相邻的癌症组织和相邻细胞系中LINC00888的表达水平。收集患者的存活预后信息,并进行了KM存活分析以确定LINC00888的预后价值。为了更好地了解LINC00888对EC细胞的增殖和迁移能力的影响,在LINC00888在欧共体细胞系中撞击后,进行细胞计数试剂盒-8(CCK-8),克隆形成和转发测定。此外,生物信息学预测网站用于发现LINC00888的潜在目标。然后,进行双荧光素酶报告基因测定以验证LINC00888和下游基因miR-34a之间的结合关系。然后,在细胞系和组织中测量两者之间的表达关系。最后,为了阐明LINC00888和MIR-34A之间的调节,使用共转染技术进行恢复实验。结果:LINC00888在食管癌组织中异常上调。存活分析表明,LINC00888的表达更高,与较短的整体存活率显着相关。细胞功能实验结果表明,LINC00888在促进EC细胞中促进肿瘤增殖和迁移能力的作用。此外,双荧光素酶报告基因测定表明miR-34a和linc00888具有结合位点。同时,我们证实,细胞和组织中miR-34a和linc00888的表达水平之间存在负相关性。细胞功能恢复实验表明,LINC00888可以通过miR-34a调节EC的进展。结论:LINC00888通过MIR-34A促进EC的增殖和迁移能力。

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