circRNA RNF111 regulates the growth, migration and invasion of gastric cancer cells by binding to miR-27b-3p

hsa_circ_0001982 [circRNA ring finger protein 111 (RNF111)] has been found to promote cancer growth; however, its role in gastric cancer (GC) remains unclear. The present study examined the effects of circR-RNF111 on the growth, migration and invasion of GC cells and aimed to elucidate the underlying molecular mechanisms. The expression levels of circR-RNF111 and miR-27b-3p in GC tissues and GC cell lines were detected by reverse transcription-quantitative PCR (RT-qPCR). StarBase v2.0 and dual-luciferase assay were used to predict and analyze the association between circR-RNF111 and miR-27b-3p. The effects of circR-RNF111 and miR-27b-3p on cell growth, apoptosis, migration and invasion were detected by cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry, wound-healing assay and Transwell assay, respectively. In addition, western blot analysis was performed to determine the expression levels of genes related to cell apoptosis and epithelial-mesenchymal transition (EMT). The results revealed that circR-RNF111 and miR-27b-3p were closely related to the clinicopathological characteristics of GC, and that circR-RNF111 and miR-27b-3p negatively correlated and were abnormally expressed in GC. circR-RNF111 acted as a sponge of miR-27b-3p. The silencing of circR-RNF111 significantly inhibited GC cell viability, colony formation, migration and invasion, and exerted a pro-apoptotic effect. miR-27b-3p inhibitor promoted the proliferation, migration and invasion of GC cells, and inhibited cell apoptosis. In addition, circR-RNF111 silencing significantly decreased the expression levels of Bcl2, Vimentin and N-cadherin, and increased those of cleaved caspase-3 and E-cadherin. Furthermore, miR-27b-3p inhibition reversed the regulatory effects of circR-RNF111 silencing on the GC cells. On the whole, the findings of the present study demonstrate that circR-RNF111 is involved in the regulation of growth, migration and invasion of GC cells by binding to miR-27b-3p.