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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

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