Long noncoding RNA LINC01703 exacerbates the malignant properties of non-small-cell lung cancer by upregulating MACC1 in a microRNA-605-3p-mediated manner
Long intergenic nonprotein coding RNA 1703 (LINC01703) has diagnostic significancein 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 itsdetailed mechanism of action. LINC01703 expression was measured by qRT-PCR. Theregulatory effects of LINC01703 on the malignancy of NSCLC cells were assessed bymultiple functional experiments. The targeted interaction was confirmed by RNAimmunoprecipitation and luciferase reporter assays. Herein, overexpression ofLINC01703 in NSCLC was indicated in the TCGA database and further proven in ourcohort. Functional studies revealed that knocking down LINC01703 repressed cellproliferation, colony formation, migration and invasion in vitro, which wasaccompanied by the induction of apoptosis. The tumor growth of LINC01703-silencedcells was also inhibited in vivo. Mechanistic analyses revealed that LINC01703functioned as a competing endogenous RNA for microRNA-605-3p (miR-605-3p) inNSCLC cells, which thereby upregulated the miR-605-3p target metastasis associatedwith colon cancer 1 (MACC1). Rescue experiments highlighted that the regulatoryactions of LINC01703 ablation on NSCLC cells were abolished in response to miR-605-3p downregulation or MACC1 overexpression. In conclusion, LINC01703enhanced the aggressiveness of NSCLC cells by altering miR-605-3p/MACC1. Ourwork suggests the therapeutic potential of LINC01703/miR-605-3p/MACC1 in NSCLC.