Abstract
Gastric cancer (GC) places a heavy burden on global health, and the information on the molecular mechanism of the progression of GC is still inadequate. Long noncoding RNA (LncRNA) has been confirmed to be widely involved in regulating the progression of GC. Our aim in this study was to explore the role and potential regulatory mechanism of lncRNA BBOX1-AS1 in GC. The expression levels of BBOX1-AS1, miR-361-3p, and MUC13 in GC tissues and cells were evaluated using quantitative real-time polymerase chain reaction and western blotting. The silencer of BBOX1 antisense RNA 1 (BBOX1-AS1) and mucin 13 (MUC13), the mimics and inhibitor of miR-361-3p, and their negative controls were used to alter the expression of these genes. Luciferase reporter, pull-down, and RNA immunoprecipitation assays were performed to verify the correlation between miR-361-3p, BBOX1-AS1, and MUC13. GC cell proliferation, invasion, and apoptosis were detected by cell counting kit-8, transwell, and flow cytometry assays, respectively. An in vivo functional experiment was performed to assess the effect of BBOX1-AS1 on GC. The results showed that BBOX1-AS1 was significantly upregulated in GC tissues. Silencing of BBOX1-AS1 inhibited GC cell proliferation and invasion and inhibited tumor growth in vivo, whereas it promoted apoptosis. MiR-361-3p was significantly downregulated in GC and counteracted the inhibitory effects of BBOX1-AS1 on GC progression. MUC13, which is targeted by miR-361-3p, is significantly upregulated in GC. MUC13 silencing inhibited GC progression was aborgated by miR-361-3p inhibitor. Collectively, BBOX1-AS1 silencing inhibits GC progression by regulating the miR-361-3p/MUC13 axis, providing a potential therapeutic biomarker for GC.