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LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1
BMC Pulmonary Medicine ( IF 3.1 ) Pub Date : 2020-03-30 , DOI: 10.1186/s12890-020-1112-3
Sen Wei , Jinghao Liu , Xin Li , Xingyu Liu

This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). Differential expression of MIR17HG in NSCLC was first detected by exploring the TCGA dataset. Expression levels of miR-142-3p in both NSCLC and non-tumor tissues were determined by qPCR. The effects of overexpressing MIR17HG on the methylation of miR-142 were assessed by MSP. The effects of overexpressing MIR17HG, miR-142-3p and Bach-1 on the invasion and migration of NSCLC cells were assessed by Trasnwell invasion or migration assay. Analysis of TCGA dataset revealed slightly downregulated expression of MIR17HG in NSCLC. This downregulation was further confirmed by measuring the expression levels of MIR17HG in NSCLC and non-tumor tissues from NSCLC patients. MIR17HG was found to decrease the methylation of miR-142-3p, and overexpression of MIR17HG led to upregulated miR-142-3p. Moreover, overexpression of MIR17HG also led to downregulated Bach-1, the downstream target of miR-142-3p. Cell invasion and migration analysis showed that overexpression of MIR17HG and miR-142-3p led to inhibited cancer cell invasion and migration. In contrast, overexpression of Bach-1 played an opposite role and attenuated the effects of overexpressing MIR17HG and miR-142-3p. MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1. TJ-MU-2012-0148594, registered January 2, 2012

中文翻译:

LncRNA MIR17HG通过上调miR-142-3p从而下调Bach-1抑制非小细胞肺癌

这项研究旨在调查MIR17HG在非小细胞肺癌(NSCLC)中的作用。首先通过探索TCGA数据集检测MIR17HG在NSCLC中的差异表达。通过qPCR测定miR-142-3p在NSCLC和非肿瘤组织中的表达水平。MSP评估了过表达的MIR17HG对miR-142甲基化的影响。通过Trasnwell侵袭或迁移分析评估过表达的MIR17HG,miR-142-3p和Bach-1对NSCLC细胞侵袭和迁移的影响。TCGA数据集的分析显示,NSCLC中MIR17HG的表达略有下调。通过测量NSCLC和来自NSCLC患者的非肿瘤组织中MIR17HG的表达水平,进一步证实了这种下调。发现MIR17HG可以降低miR-142-3p的甲基化,MIR17HG的过表达导致miR-142-3p上调。此外,MIR17HG的过度表达还导致下调Bach-1(miR-142-3p的下游靶标)。细胞侵袭和迁移分析表明,MIR17HG和miR-142-3p的过度表达导致癌细胞的侵袭和迁移受到抑制。相反,Bach-1的过度表达则起相反的作用,并减弱了过表达MIR17HG和miR-142-3p的作用。MIR17HG通过上调miR-142-3p从而下调Bach-1来抑制NSCLC。TJ-MU-2012-0148594,2012年1月2日注册 Bach-1的过表达起相反的作用,并减弱了过表达的MIR17HG和miR-142-3p的作用。MIR17HG通过上调miR-142-3p从而下调Bach-1来抑制NSCLC。TJ-MU-2012-0148594,2012年1月2日注册 Bach-1的过表达起相反的作用,并减弱了过表达MIR17HG和miR-142-3p的作用。MIR17HG通过上调miR-142-3p从而下调Bach-1来抑制NSCLC。TJ-MU-2012-0148594,2012年1月2日注册
更新日期:2020-04-22
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