CircPRDM5 inhibits the proliferation, migration, invasion, and glucose metabolism of gastric cancer cells by reducing GCNT4 expression in a miR‐485‐3p‐dependent manner

Abstract

AbstractCircular RNA (circRNA) plays a key part in the pathological process of gastric cancer (GC). The study is organized to analyze the function of circPRDM5 in GC cell tumor properties. Expression levels of circPRDM5, miR‐485‐3p, glucosaminyl (N‐acetyl) transferase 4 (GCNT4), ki67, E‐cadherin, N‐cadherin, and hexokinase 2 (HK2) were analyzed by quantitative real‐time polymerase chain reaction (PCR), Western blotting or immunohistochemistry assay. Cell proliferation was assessed by cell colony formation assay and 5‐ethynyl‐2′‐deoxyuridine assay. Cell migration and invasion were investigated by transwell assay. Glycolysis was evaluated by the Seahorse XF Glycolysis Stress Test Kit. Dual‐luciferase reporter assay and RNA pull‐down assay were performed to identify the associations among circPRDM5, miR‐485‐3p, and GCNT4. Xenograft mouse model assay was conducted to determine the effects of circPRDM5 on tumor formation in vivo. CircPRDM5 and GCNT4 expression were downregulated, while miR‐485‐3p expression was upregulated in GC tissues and cells when compared with paracancerous tissues or human gastric epithelial cells. CircPRDM5 overexpression inhibited proliferation, migration, invasion, and glucose metabolism of GC cells; however, circPRDM5 depletion had the opposite effects. CircPRDM5 repressed tumor properties of GC cells in vivo. MiR‐485‐3p restoration relieved circPRDM5‐induced effects in GC cells. GCNT4 overexpression remitted the promoting effects of miR‐485‐3p mimics on GC cell malignancy. CircPRDM5 acted as a sponge for miR‐485‐3p, and GCNT4 was identified as a target gene of miR‐485‐3p. Moreover, circPRDM5 regulated GCNT4 expression by interacting with miR‐485‐3p.CircPRDM5 acted as a miR‐485‐3p sponge to inhibit GC progression by increasing GCNT4 expression, proving a potential target for GC therapy.