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The present study aimed to assess the role of the long non-coding RNA-urothelial cancer associated 1 (lncRNA-UCA1)/microRNA (miR)-383/vascular endothelial growth factor A (VEGFA) axis in regulating lung adenocarcinoma physiology through  in vivo  and  in vitro  experiments. The expression profile of lncRNA-UCA1 was analyzed by genome-wide analysis from GSE146459. The cell counting Kit-8, colony formation, wound healing and transwell assays were performed to evaluate the effects of lncRNA-UCA1  in vitro . In addition, luciferase reporter assays were performed to confirm the binding site. The expression levels of miR-383 and VEGFA in tumor cells were measured using reverse transcription-quantitative PCR. HCC-78 was also transfected with miR-383 mimics, inhibitors and siRNA-VEGFA before their viability was also assessed. Xenograft models were established in nude mice to investigate the tumor characteristics  in vivo . The expression of lncRNA-UCA1 was significantly increased in tumor tissues and cells compared with adjacent tissues or HBE cells. Silencing lncRNA-UCA1 expression in cells resulted in a reduction in lung cancer cell viability. In addition, lncRNA-UCA1 silencing increased the expression of miR-383. Inhibiting miR-383 expression increased HCC-78 proliferation, migration and invasion, whilst reducing their apoptosis. miR-383 was shown to specifically target VEGFA to inhibit its expression at both the protein and mRNA levels. VEGFA knockdown resulted in a reduction in all aforementioned aspects of HCC-78 cell activity. In addition, inhibiting miR-383 expression led to larger tumor sizes  in vivo . To conclude, the results of the study suggest that lncRNA-UCA1 can regulate the expression of miR-383 and, in turn, VEGFA.

LncRNA-UCA1 regulates lung adenocarcinoma progression through competitive binding to miR-383