Abstract
The important functions of long non‑coding RNAs in the malignancy of non‑small cell lung cancer (NSCLC) has been increasingly highlighted. However, whether LINC01748 functions in a crucial regulatory role still requires further research. The aim of the present study was to investigate the biological roles of LINC01748 in NSCLC. Furthermore, different experiments were utilized to investigate the mechanism of action of LINC01748 in 2 NSCLC cell lines. Reverse transcription‑quantitative PCR was used to measure mRNA expression levels. Cell Counting Kit‑8 assay, flow cytometry analysis and Transwell and Matrigel assays were also used to analyze, cell viability, apoptosis, and migration and invasion, respectively. A tumor xenograft model was used for in vivo experiments. RNA immunoprecipitation experiments, luciferase reporter assays and rescue experiments were used to investigate the mechanisms involved. Data from The Cancer Genome Atlas dataset and patients recruited into the present study showed that LINC01748 was overexpressed in NSCLC. Patients with high LINC01748 mRNA expression level had shorter overall survival rate compared with that in patients with low LINC01748 mRNA expression level. Then, knockdown of LINC01748 mRNA expression level reduced cell proliferation, migration and invasion, but increased cell apoptosis in vitro. Knockdown of LINC01748 also reduced tumor growth in vivo. Mechanistically, LINC01748 could act as a competing endogenous (ce)RNA to sponge microRNA(miR)‑520a‑5p, to increase the expression level of the target gene, high mobility group AT‑hook 1 (HMGA1) in the NSCLC cell lines. Furthermore, rescue experiments illustrated that the functions exerted by LINC01748 knockdown were negated by miR‑520a‑5p inhibition or HMGA1 overexpression. In summary, LINC01748 acted as a ceRNA by sponging miR‑520a‑5p, leading to HMGA1 overexpression, thus increasing the aggressiveness of the NSCLC cells. Accordingly, targeting the LINC01748/miR‑520a‑5p/HMGA1 pathway may benefit NSCLC therapy.