Background: Gastric cancer (GC) ranks third among the causes of cancer-related deaths in the world. Circular RNA hsa_circ_0021087 (circ_0021087) plays a repressive role in GC. Nevertheless, the mechanism by which circ_0021087 constrains GC advancement is unclear.
Materials and methods: Expression patterns of circ_0021087, microRNA (miR)-184 and FBJ murine osteosarcoma viral oncogene homolog B (FOSB) mRNA were assessed by quantitative real-time polymerase chain reaction (RT-qPCR). Gain-of-function experiments were conducted to verify the biological function of circ_0021087 in vitro and in vivo, including cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell and xenograft assays. Protein levels were analysed by Western blotting and immunohistochemistry (IHC). The regulatory mechanism of circ_0021087 was analysed by bioinformatics analysis, dual-luciferase reporter and RNA immunoprecipitation (RIP) assays.
Results and conclusion: Circ_0021087 and FOSB were lowly expressed in GC, whereas miR-184 had an opposite result. Circ_0021087 overexpression repressed GC cell proliferation and epithelial-mesenchymal transition (EMT) in xenograft models in vivo and induced GC cell apoptosis, repressed GC cell proliferation, EMT, migration and invasion in vitro. Circ_0021087 could elevate FOSB expression by adsorbing miR-184. MiR-184 mimic reversed the inhibitory influence of circ_0021087 overexpression on GC cell malignancy. Also, FOSB knockdown offset the suppressive impact of miR-184 silencing on GC cell malignancy. In conclusion, circ_0021087 played a repressive influence on GC progression by elevating FOSB expression by adsorbing miR-184, offering a new mechanism for circ_0021087 to inhibit the progression of GC.
Keywords: FOSB; GC; circ_0021087; miR-184.
© 2021 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.