Abstract
Dysregulated long non-coding RNAs (lncRNAs) play an important role in cancer progression. However, there have been limited reports to date of the involvement of ubiquitin-binding protein domain protein 10 antisense RNA 1 (UBXN10-AS1) in cancer. Our aim was to explore the role and underlying mechanism of UBXN10-AS1 in the occurrence of colon adenocarcinoma (COAD). Real-time quantitative PCR and Western blotting were performed to determine the expression of UBXN10-AS1, miR-515-5p, and Slit guidance ligand 3 (SLIT3). Cell Counting Kit-8 and wound healing scratch assays were performed to measure COAD cell proliferation and migration. A xenograft assay was performed to examine tumor growth in vivo. Luciferase reporter and RNA immunoprecipitation (RIP) assays were used to determine the binding interaction among miR-515-5p, UBXN10-AS1, and SLIT3. The results showed that UBXN10-AS1 and SLIT3 were expressed at low levels in COAD tissues, while miR-515-5p was expressed at high levels. UBXN10-AS1 overexpression suppressed tumor growth in vitro and in vivo. The luciferase reporter and RNA RIP assays demonstrated that UBXN10-AS1 targeted miR-515-5p, which in turn targeted SLIT3. Functionally, miR-515-5p overexpression reversed the inhibition of COAD cell proliferation and migration by UBXN10-AS1 overexpression, and SLIT3 overexpression counteracted the oncogenicity of miR-515-5p. Our study shows that UBXN10-AS1 modulates the miR-515-5p/SLIT3 axis, thereby resulting in the inhibition of COAD cell proliferation and migration.