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miR-628-5p promotes growth and migration of osteosarcoma by targeting IFI44L.
Biochemistry and Cell Biology ( IF 2.4 ) Pub Date : 2019-04-24 , DOI: 10.1139/bcb-2019-0001
Ju-Yong Wang 1 , Ju-Qiang Wang 2 , Shi-Bao Lu 1
Affiliation  

This study investigated the role of miR-628-5p and interferon-induced protein 44-like (IFI44L) in osteosarcoma (OS) and determined whether miR-628-5p modulated OS growth by regulating IFI44L. Based on the data downloaded from Gene Expression Omnibus (GEO) database, we revealed that the expression of IFI44L was downregulated in OS and low expression of IFI44L was correlated with better prognosis of patients with OS. Biological prediction of its upstream regulatory miRNAs on the miRWalk website found that miR-628-5p is a possible upstream regulatory miRNA of IFI44L. Luciferase activity assay demonstrated that miR-628-5p could bind to the 3' untranslated region (UTR) of IFI44L, which proved the above prediction. The expression of miR-628-5p is upregulated in OS and high expression of miR-628-5p is correlated with poor prognosis of patients with OS. The results of RT-qPCR showed that the expression of miR-628-5p in MG-63, U2OS, Saos-2, and SW1353 cells was significantly higher than that in the hFOB1.19 cells. Downregulation of miR-628-5p by miR-628-5p inhibitor significantly inhibited the proliferation, migration, and invasion of MG-63 cells. By rescue assay, we found that knockdown of IFI44L rescued the proliferation and motility of miR-628-5p depleted MG-63 cells. Collectively, our present data illustrated that miR-628-5p promoted the growth and motility of OS at least partly by targeting IFI44L. Moreover, miR-628-5p and IFI44L might be proposed as promising biomarkers in OS diagnosis and treatment.

中文翻译:

miR-628-5p通过靶向IFI44L促进骨肉瘤的生长和迁移。

这项研究调查了miR-628-5p和干扰素诱导的蛋白44-样(IFI44L)在骨肉瘤(OS)中的作用,并确定miR-628-5p是否通过调节IFI44L来调节OS生长。根据从Gene Expression Omnibus(GEO)数据库下载的数据,我们发现IFI44L的表达在OS中被下调,而IFI44L的低表达与OS患者的更好预后相关。在miRWalk网站上对其上游调控miRNA的生物学预测发现,miR-628-5p是IFI44L可能的上游调控miRNA。萤光素酶活性测定表明,miR-628-5p可以与IFI44L的3'非翻译区(UTR)结合,证明了上述预测。miR-628-5p的表达在OS中上调,而miR-628-5p的高表达与OS患者的不良预后相关。RT-qPCR结果表明,miR-628-5p在MG-63,U2OS,Saos-2和SW1353细胞中的表达明显高于在hFOB1.19细胞中的表达。miR-628-5p抑制剂对miR-628-5p的下调显着抑制了MG-63细胞的增殖,迁移和侵袭。通过抢救测定,我们发现IFI44L的敲除拯救了miR-628-5p耗尽的MG-63细胞的增殖和运动。总的来说,我们目前的数据表明,miR-628-5p至少部分通过靶向IFI44L促进了OS的生长和运动。此外,miR-628-5p和IFI44L可能被建议作为OS诊断和治疗中有希望的生物标志物。RT-qPCR结果表明,miR-628-5p在MG-63,U2OS,Saos-2和SW1353细胞中的表达明显高于在hFOB1.19细胞中的表达。miR-628-5p抑制剂对miR-628-5p的下调显着抑制了MG-63细胞的增殖,迁移和侵袭。通过抢救测定,我们发现IFI44L的敲除拯救了miR-628-5p耗尽的MG-63细胞的增殖和运动。总的来说,我们目前的数据表明,miR-628-5p至少部分通过靶向IFI44L促进了OS的生长和运动。此外,miR-628-5p和IFI44L可能被建议作为OS诊断和治疗中有希望的生物标志物。RT-qPCR结果表明,miR-628-5p在MG-63,U2OS,Saos-2和SW1353细胞中的表达明显高于在hFOB1.19细胞中的表达。miR-628-5p抑制剂对miR-628-5p的下调显着抑制了MG-63细胞的增殖,迁移和侵袭。通过抢救测定,我们发现IFI44L的敲除拯救了miR-628-5p耗尽的MG-63细胞的增殖和运动。总的来说,我们目前的数据表明,miR-628-5p至少部分通过靶向IFI44L促进了OS的生长和运动。此外,miR-628-5p和IFI44L可能被建议作为OS诊断和治疗中有希望的生物标志物。miR-628-5p抑制剂对miR-628-5p的下调显着抑制了MG-63细胞的增殖,迁移和侵袭。通过抢救测定,我们发现IFI44L的敲除拯救了miR-628-5p耗尽的MG-63细胞的增殖和运动。总的来说,我们目前的数据表明,miR-628-5p至少部分通过靶向IFI44L促进了OS的生长和运动。此外,miR-628-5p和IFI44L可能被建议作为OS诊断和治疗中有希望的生物标志物。miR-628-5p抑制剂对miR-628-5p的下调显着抑制了MG-63细胞的增殖,迁移和侵袭。通过抢救测定,我们发现IFI44L的敲除拯救了miR-628-5p耗尽的MG-63细胞的增殖和运动。总的来说,我们目前的数据表明,miR-628-5p至少部分通过靶向IFI44L促进了OS的生长和运动。此外,miR-628-5p和IFI44L可能被建议作为OS诊断和治疗中有希望的生物标志物。
更新日期:2019-11-01
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