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miR-101-3p and miR-199b-5p promote cell apoptosis in oral cancer by targeting BICC1.
Molecular and Cellular Probes ( IF 3.3 ) Pub Date : 2020-04-04 , DOI: 10.1016/j.mcp.2020.101567
Hong Wang 1 , Ying Guo 1 , Nu Mi 2 , Liwei Zhou 3
Affiliation  

microRNAs (miRNAs) are involved in the carcinogenesis and progression of oral cancer. In this research, we aimed to identify the DE_miRNAs in oral cancer and the related molecular mechanisms. Using the GEO2R online tool, we identified 19 DE_miRNAs from the GSE115117 dataset and 3343 the DEGs from GSE74530 dataset. GO enrichment analysis of DE_miRNAs were performed using FunRich online analysis. Venn diagrams of the overlapping genes regulated by miR-204-5p, miR-199b-5p, and miR-101-3p were constructed using Draw Venn Diagram, FunRich, miRDB, TargetScan and GSE74530 databases. Cytoscape was used to construct a miRNAs-mRNAs network. RT-PCR and western blotting showed downregulation of miR-199b-5p and miR-101-3p, and upregulation of BICC1 in oral cancer cell lines and tissues. Spearman correlation analysis further demonstrated a positive correlation between miR-101-3p and miR-199b-5p levels and that miR-199b-5p and miR-101-3p were negatively correlated with BICC1 mRNA levels. miR-199b-5p and BICC1 were significantly related to survival rate of patients with oral cancer. Upregulation of miR-199b-5p and miR-101-3p inhibited the viability and promoted the apoptosis in TSCCA and SCC-9 cells, as shown by the CCK8 assay and flow cytometry analysis, respectively. Inhibition of BICC1 reduced viability and promoted apoptosis in TSCCA cells. Additionally, the relationship between BICC1 and both miR-101-3p and miR-199b-5p was assessed by a luciferase reporter assay. The effects of miR-101-3p and miR-199b-5p upregulation on the promotion of cell apoptosis and the inhibition of tumor growth were reversed by overexpression of BICC1. In conclusion, the increased levels of miR-199b-5p and miR-101-3p enhanced apoptosis and suppressed cell viability in oral cancer by suppressing BICC1 expression.

中文翻译:

miR-101-3p和miR-199b-5p通过靶向BICC1促进口腔癌中的细胞凋亡。

microRNA(miRNA)参与口腔癌的发生和发展。在这项研究中,我们旨在鉴定口腔癌中的DE_miRNA及其相关的分子机制。使用GEO2R在线工具,我们从GSE115117数据集中识别出19个DE_miRNA,从GSE74530数据集中识别了3343个DEG。使用FunRich在线分析进行DE_miRNA的GO富集分析。使用Draw Venn Diagram,FunRich,miRDB,TargetScan和GSE74530数据库构建了miR-204-5p,miR-199b-5p和miR-101-3p调控的重叠基因的Venn图。Cytoscape用于构建miRNA-mRNA网络。RT-PCR和蛋白质印迹显示在口腔癌细胞系和组织中miR-199b-5p和miR-101-3p的下调以及BICC1的上调。Spearman相关分析进一步证明了miR-101-3p和miR-199b-5p水平呈正相关,而miR-199b-5p和miR-101-3p与BICC1 mRNA水平呈负相关。miR-199b-5p和BICC1与口腔癌患者的生存率显着相关。分别由CCK8分析和流式细胞仪分析表明,miR-199b-5p和miR-101-3p的上调抑制了TSCCA和SCC-9细胞的活力并促进了其凋亡。抑制BICC1降低了TSCCA细胞的活力并促进了其凋亡。此外,BICC1与miR-101-3p和miR-199b-5p之间的关系通过萤光素酶报告基因分析进行了评估。BICC1的过表达逆转了miR-101-3p和miR-199b-5p上调对促进细胞凋亡和抑制肿瘤生长的作用。
更新日期:2020-04-04
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