Long noncoding RNA LINC00858 promotes the proliferation, migration and invasion of gastric cancer cells via the miR-363-3p/FOXP4 axis.

Abstract

Long non-coding RNA (lncRNA) LINC00858 has been found to exert oncogenic activity in several types of cancers, except gastric cancer (GC). In the present study, we aimed to explore the potential role of LINC00858 in GC and the underlying molecular mechanism. The expression patterns of LINC00858 were determined using qRT-PCR in GC samples and cell lines. Cell proliferation was examined utilizing CCK-8 assay. Cell migration and invasion were evaluated using transwell assays. We used the bioinformatics software StarBase and TargetScan to predict lncRNA-miRNA and miRNA-mRNA interactions. Our findings revealed that LINC00858 expression was markedly upregulated in GC tissues and cell lines. Loss-of-function experiments demonstrated that LINC00858 silencing inhibited the proliferation, migration and invasion of GC cells. Bioinformatics analysis showed that there were several complementary binding sites between LINC00858 and microRNA (miR)-363-3p, and further Luciferase reporter assay confirmed the interaction between LINC00858 and miR-363-3p. In addition, forkhead box P4 protein (FOXP4) was found to be a target gene of miR-363-3p in GC cells. FOXP4 overexpression reversed the inhibitory effects of miR-363-3p mimics on cell proliferation, migration and invasion of BGC-823 cells. Collectively, LINC00858 acted as an oncogene in GC via regulating miR-363-3p/FOXP4 axis, which indicated that LINC00858 might be a novel therapeutic target for the treatment of GC.