Abstract
Long intergenic nonprotein-coding RNA 1703 (LINC01703) has diagnostic significance in lung adenocarcinoma. However, its specific roles in non-small cell lung cancer (NSCLC) and downstream mechanisms have not been investigated. In the current study, we characterized the role of LINC01703 in NSCLC malignancy and elucidated its detailed mechanism of action. LINC01703 expression was measured by qRT-PCR. The regulatory effects of LINC01703 on the malignancy of NSCLC cells were assessed by multiple functional experiments. The targeted interaction was confirmed by RNA immunoprecipitation and luciferase reporter assays. Herein, overexpression of LINC01703 in NSCLC was indicated in the TCGA database and further proven in our cohort. Functional studies revealed that knocking down LINC01703 repressed cell proliferation, colony formation, migration, and invasion in vitro, which was accompanied by the induction of apoptosis. The tumor growth of LINC01703-silenced cells was also inhibited in vivo. Mechanistic analyses revealed that LINC01703 functioned as a competing endogenous RNA for microRNA-605-3p (miR-605-3p) in NSCLC cells, which thereby upregulated the miR-605-3p target metastasis associated with colon cancer 1 (MACC1). Rescue experiments highlighted that the regulatory actions of LINC01703 ablation on NSCLC cells were abolished in response to miR-605-3p downregulation or MACC1 overexpression. In conclusion, LINC01703 enhanced the aggressiveness of NSCLC cells by altering miR-605-3p/MACC1. Our work suggests the therapeutic potential of LINC01703/miR-605-3p/MACC1 in NSCLC.