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Introduction
Currently, lung cancer is one of the most common, aggressive, and deadly malignant tumors worldwide [1]. Especially with the aging of population, lung cancer is a serious public health problem in older adults. Lung cancer can be broadly divided into two major tissue subtypes: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), and the former accounts for about 85% of lung cancer [2]. Lung adenocarcinoma (LUAD) is the most common and fatal subtype of NSCLC [3]. Although the diagnosis and treatment of lung cancer has improved recently, most patients are already in the middle and late stages with distant metastases and poor prognosis due to the lack of early and effective screening tool. Furthermore, recent studies have found that lung cancer is a disease of molecular heterogeneity, with a variety of gene mutations and epigenetic changes [3, 4]. Therefore, it is important to understand the molecular mechanisms of lung adenocarcinoma in order to develop targeted therapies with optimal efficacy.
MicroRNAs (miRNAs) are endogenous, small molecule single-stranded non-coding RNAs that exist in eukaryotes, which are approximately 22 nucleotides in length [5]. Mature miRNAs interfere with mRNA translation and promote mRNA degradation by binding to complementary base sequences in the 3' non-coding region of target gene messenger RNA (mRNA) and then regulate gene expression at the post-transcriptional level [6]. It has been reported that miRNAs regulate up to 60% of human genes, and participate in various pathological processes, including tumorigenesis [7] . In recent years, increasing data have shown that aberrant miRNA expression not only promotes the occurrence and metastasis of lung cancer, but also impacts the survival rate of lung cancer patients [8].
miR-17-5p is one of the most studied members of the miR-17–92 gene cluster and plays an important role as an oncogene or tumor suppressor in various human cancers [9, 10]. The expression of miR-17-5p was significantly higher in lung cancer tissues compared with adjacent normal tissues [10]. However, the mechanism of action of miR-17-5p in lung adenocarcinoma is not completely understood. In this study, we found that miR-17-5p was highly expressed in human lung adenocarcinoma cells compared with normal human lung epithelial cells. Upregulation of miR-17-5p significantly promoted the proliferation, invasion, and migration of lung adenocarcinoma cells and inhibited...