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.