Lung cancer is considered as the leading cause of cancer-related mortality for decades worldwide [
1]. The latest GLOBOCAN statistics reported that lung cancer caused 1,761,007 deaths, accounting for 18.4% of all cancer deaths in 2018 [
2]. In the same year, there were 2,093,876 new cases of lung cancer, accounting for 11.6% of all new cancer cases [
2]. It is estimated that more than 50% of lung cancer patients diagnosed with a localized tumor can live longer than 5 years, but only 16% of lung cancer patients are diagnosed at early stages [
3]. Once distant metastasis occurs, only 6% of lung cancer patients can survive for 5 years [
4]. Tobacco smoking is responsible for the majority of lung cancer cases, while this disease also affects never-smokers, indicating the complicated pathogenesis [
5,
6]. Studies on the molecular mechanisms of lung cancer have identified critical molecular pathways involved in the development and progression of this disease [
7,
8]. Characterization of lncRNAs involved in lung cancer provides novel insights into the development of targeted therapies [
9,
10]. Non-coding RNAs (ncRNAs), such as long (> 200 nt) ncRNAs (lncRNAs) [
11] and miRNAs [
12] are critical players in cancer biology and either promote or suppress cancer development by regulating the expression of cancer-related genes. Therefore, regulating the expression of cancer-related ncRNAs may benefit cancer treatment. However, the functions of most ncRNAs in cancer remain unclear. PSMG3-AS1 was recently characterized as an oncogenic lncRNA in breast cancer [
13], while its role in lung cancer remains unclear. Our bioinformatics analysis showed that PSMG3-AS1 may be targeted by miR-449b-5p, which is a tumor suppressive miRNA [
14]. This study was therefore carried out to investigate the interaction between miR-449b-5p and PSMG3-AS1 in lung adenocarcinoma, a major subtype of lung cancer.