Hsa_circ_0000026 Sponges miR-23a-5p and Upregulates PTEN Expression to Suppress Gastric Cancer Cell Progression

Abstract

Abstract The role of circular RNAs (ciRNAs; whose dysregulation causes various cancer types) in gastric cancer (GC) remains largely unknown. Here, we investigated the expression of a ciRNA, hsa_circ_0000026 (ciR-0026), in GC tissues and deciphered the molecular mechanism by which ciR-0026 suppresses GC cell proliferation. ciR-0026 expression in GC cells was analyzed using quantitative PCR. The clinical significance of the changes in ciR-0026 expression in GC cells was analyzed using the SPSS.25 software. The effects of ciR-0026overexpression on GC cell phenotypes were determined using colony formation, cell counting kit-8, and transwell assays. Additionally, biotin-coupled probe RNA pull-down and dual-luciferase reporter assays were performed. ciR-0026 expression was downregulated in 90.5% (57/63) of the primary GC tissues compared with that in the adjacent gastric mucosal tissues (p< 0.05). The expression of ciR-0026 was affected by tumor differentiation, lymph node metastasis, and tumor node metastasis stage (p < 0.05). An increase in ciR-0026 expression suppressed GC cell proliferation and invasion in vitro. Mechanistically, ciR-0026 acted as a sponge for microRNA (miR)-23a-5p, which directly targeted the phosphate and tension homology deleted on chromosome ten (PTEN) gene. The proliferative, invasive, and migratory abilities of GC cells were inhibited by ciR-0026 upregulation. Moreover, high ciR-0026 levels inhibited epithelial-to-mesenchymal transition of GC cells via the modulation of the miR-23a-5p/PTEN axis; however, suppressing PTENexpression reversed these effects. In conclusion, ciR-0026 may be a potential prognostic biomarker of GC, serving as a suppressor of GC via the miR-23a-5p/PTEN axis.