Abstract
Long non-coding RNAs (lncRNAs) have been reported to participate in multiple biological processes, including tumorigenesis. In the current study, the function of a novel lncRNA LINC00887 was investigated in lung carcinoma. For this purpose, LINC00887 expression was assessed by reverse-transcription quantitative PCR. Cell viability was determined by the CCK-8 and EdU assays. Cell invasion, migration were assessed by the transwell and wound healing assays, respectively. A dual luciferase assay was used for analysis of the interaction between LINC00887 and miR-206, as well as the relationship of miR-206 with NRP1. A tumor xenograft study was performed to investigate the LINC00887-miR-206-NRP1 axis in vivo. The expression levels of LINC00887 were upregulated in lung carcinoma tissues and cells compared with adjacent tissues or normal cells (BEAS-2B). Knockdown LINC00887 significantly inhibited the proliferation, migration and invasion of lung carcinoma A549 and NCI-H460 cells. Furthermore, LINC00887 was identified as a competing endogenous RNA and to directly interact with miR-206. Mechanistically, miR-206 was demonstrated to regulate neuropilin-1 (NRP1) expression by targeting the NRP1 3'-untranslated region. The results of the present study suggested that the LINC00887-miR-206-NRP1 axis served a critical role in regulating lung carcinoma cell proliferation, migration and invasion. In addition, xenograft tumor model experiments revealed that silencing LINC00887 suppressed lung carcinoma tumor growth of in vivo. In summary, our results suggest that LINC00887 may serve an oncogenic role in lung carcinoma by targeting the miR-206/NRP1 axis, providing a potential therapeutic target for patients with lung carcinoma.