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

ABSTRACT: 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.

SUBMITTER: Wang Z

PROVIDER: S-EPMC7521560 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe aberrant expression of circular RNAs (circRNAs) plays vital roles in the advancement of human cancers, including gastric cancer (GC). In this study, the functions of circRNA ring finger protein 111 (circ-RNF111) in GC were investigated.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) assay was performed for the levels of circ-RNF111, microRNA-876-3p (miR-876-3p) and krueppel-like factor 12 (KLF12) mRNA. RNase R assay was conducted for the feature of circ-RNF111. Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound-healing assay, and transwell assay were applied for cell viability, colony formation, migration, and invasion, respectively. Flow cytometry analysis was used to analyze cell apoptosis and cell cycle process. The glycolysis level was examined using specific commercial kits. Western blot assay was carried out to measure the protein levels of hexokinase 2 (HK-2) and KLF12. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to verify the combination between miR-876-3p and circ-RNF111 or KLF12. Murine xenograft model was constructed for the role of circ-RNF111 in vivo. Immunohistochemistry (IHC) was used for KLF12 level.ResultsCirc-RNF111 was higher expressed in GC tissues and cells than normal tissues and cells. Silencing of circ-RNF111 restrained cell viability, colony formation, migration, invasion, cell cycle process and glycolysis and induced apoptosis in GC cells in vitro. Circ-RNF111 positively regulated KLF12 expression via absorbing miR-876-3p. MiR-876-3p downregulation reversed the impacts of circ-RNF111 silencing on GC cell malignant phenotypes. MiR-876-3p overexpression repressed GC cell growth, metastasis and glycolysis, inhibited apoptosis and arrested cell cycle, while KLF12 elevation weakened the effects. Besides, circ-RNF111 knockdown inhibited tumor growth in vivo.ConclusionCirc-RNF111 knockdown relieved the development of GC by regulating miR-876-3p/KLF12 axis.

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

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