Lung cancer has been the most common type of malignancy that causes the highest mortality rate among all types of malignancies for decades [
1]. In 2018, lung cancer affected 11.6% (2,093,876 cases) of all newly diagnosed cancer cases and caused 18.4% (1,761,007 cases) of all cancer deaths [
2]. Avoidance of smoking and second-hand smoking can significantly reduce the risk of lung cancer [
3]. However, to quit smoking, it requires intensive intervention for smokers’ life. More importantly, lung cancer also affects never-smokers [
4]. The current survival of lung cancer patients is still poor, largely due to the lack of effective therapies for advanced lung cancer and the low rate of early diagnosis [
5,
6].
Genetic factors play central roles in the pathogenesis of lung cancer [
7]. The identification of genetic factors involved in this disease provided potential targets for the development of targeted therapies [
8,
9]. Non-coding RNAs (ncRNAs) have no protein-coding capacity but affect protein synthesis by regulating gene expression [
10]. For instance, long (> 200 nt) non-coding RNAs (lncRNAs) are usually spatially expressed and affect local gene expression [
11]. However, the functions of most lncRNAs in cancer remain unclear. LncRNA miR-17-92a-1 cluster host gene (MIR17HG) has been reported to produce cancer-related miRNAs [
12]. For instance, MIR17HG produces miRNA-19a/b to mediate the anti-neoplastic effects induced by grape seed procyanidin extract in the treatment of lung cancer [
13]. MIR17HG was also reported to promote colorectal cancer by interacting with miR-17-5p [
14]. In the present study, we observed downregulated expression pattern of MIR17HG in NSCLC by analyzing TCGA dataset. In addition, our preliminary deep sequencing data revealed positive correlation between the expression of MIR17HG and miR-142-3p, a tumor suppressive miRNA [
15], across NSCLC tissue samples (data not shown). This study aimed to investigate the potential involvement of MIR17HG in non-small cell lung cancer (NSCLC), a major subtype of lung cancer, and explore its possible interactions with miR-142-3p.