LINC01094 promotes the invasion of ovarian cancer cells and regulates the Wnt/β-catenin signaling pathway by targeting miR-532-3p

Long non-coding RNAs (lncRNAs) participate in the development of ovarian cancer (OC). The present study aimed to explore the roles of long intergenic non-protein coding RNA 1094 (LINC01094) in OC. LINC01094 and microRNA (miR)-532-3p expression in OC tissues and cells were measured using reverse transcription-quantitative PCR. Cell migration and invasion were detected using wound healing assays and Transwell assays, respectively. The binding of LINC01094 or beta-catenin to miR-126-5p was detected using a Dual-luciferase reporter assay, and protein expression was confirmed using western blot analysis. The expression level of LINC01094 in patients with OC was higher in OC tissues compared with in adjacent tissues, and LINC01094 was upregulated in OC cell lines. In addition, LINC01094 overexpression promoted the viability, migration, invasion and cell cycle progression of OC cells, and inhibited OC cell apoptosis. Moreover, LINC01094 negatively regulated miR-532-3p in OC cells and tissues. miR-532-3p overexpression decreased the viability, migration, invasion and cell cycle progression of OC cells alongside downregulation of Wnt/beta-catenin signaling pathway protein expression, as well as increasing OC cell apoptosis. Inhibition of LINC01094 with small interfering (si)-LINC01094 and overexpression of LINC01094 respectively reversed the effect of miR-532-3p inhibitor and mimics on OC cells. miR-532-3p could directly target beta-catenin, and miR-532-3p inhibitor increased beta-catenin expression, while si-LINC01094 attenuated this effect. In addition, LINC01094 overexpression promoted tumor growth in vivo by regulating miR-532-3p. Taken together, LINC01094 promoted the growth, migration, invasion and Wnt/beta-catenin signaling pathway expression of OC cells by modulating miR-532-3p.