Circ_0003789 Facilitates Gastric Cancer Progression by Inducing the Epithelial-Mesenchymal Transition through the Wnt/β-Catenin Signaling Pathway

Background: The role of circular RNAs in the pathogenesis of gastric cancer (GC) has been well documented by numerous studies. However, whether circ_0003789 plays a role during GC progression remains to be determined. Thus, this study aimed to investigate the biological functions of circ_0003789 during GC progression. Materials and Methods: Circ_0003789 expression was determined using quantitative real-time polymerase chain reaction in GC and matched para-carcinoma normal tissues. Functional experiments were performed to estimate changes in the proliferation, apoptosis, migration, and invasion of GC cells treated to silence circ_0003789. E-cadherin, vimentin, Wnt3a, and beta-catenin expression was determined using immunofluorescence staining and western blot assays. Xenograft tumor growth and Ki67 expression were also evaluated in vivo. Results: Circ_0003789 was upregulated in GC tissues and cells, and its upregulation positively correlated with poor tumor differentiation, distal metastasis, and advanced clinical stage. Silencing circ_0003789 inhibited GC cell proliferation, migration, invasion, and the epithelial-mesenchymal transition (EMT), both in vitro and in vivo. Mechanistically, the Wnt/beta-catenin signaling pathway was repressed by circ_0003789 silencing. Conclusions: Circ_0003789 facilitates GC progression by inducing the EMT through the Wnt/beta-catenin signaling pathway.

Automated summary

This study found that circ_0003789 is upregulated in gastric cancer and is positively associated with tumor differentiation, distal metastasis, and advanced clinical stage. Silencing circ_0003789 can inhibit gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition, possibly through the repression of the Wnt/beta-catenin signaling pathway.