LncRNA MIR17HG inhibits non-small cell lung cancer by upregulating miR-142-3p to downregulate Bach-1.

ABSTRACT

BACKGROUND: This study aimed to investigate the role of MIR17HG in non-small cell lung cancer (NSCLC). METHODS: 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. RESULTS: 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. CONCLUSION: MIR17HG inhibits NSCLC by upregulating miR-142-3p to downregulate Bach-1. TRIAL REGISTRATION TJ-MU-2012-0148594, registered January 2, 2012.