circRNA TATA‐box binding protein associated factor 15 acts as an oncogene to facilitate bladder cancer progression through targeting miR‐502‐5p/high mobility group box 3

Abstract Circular RNAs (circRNAs) are key in regulating bladder cancer progression. This study explored the effects of circRNA TATA‐box binding protein associated factor 15 (circTAF15) on bladder cancer progression. We enrolled 80 bladder cancer patients to examine the relationship between circTAF15 expression and clinical features. The function of circTAF15 on bladder cancer cell viability, proliferation, migration, invasion, and glycolysis was monitored by cell counting kit‐8 assay, 5‐Ethynyl‐2′‐deoxyuridine experiment, Transwell experiment, and glycolysis analysis. Dual luciferase reporter gene assay, RNA pull‐down assay, and RNA immunoprecipitation assay were used to verify the binding between circTAF15 and miR‐502‐5p or between miR‐502‐5p and high mobility group box 3 (HMGB3). circTAF15 effect on in vivo growth of bladder cancer was investigated by xenograft tumor experiment. Quantitative real‐time polymerase chain reaction, Western blot, and immunohistochemistry were implemented to investigate the expression levels of genes. circTAF15 was upregulated in bladder cancer patients, associated with unfavorable outcomes. circTAF15 knockdown attenuated bladder cancer cell viability, proliferation, migration, invasion, epithelial‐mesenchymal transition, and glycolysis. circTAF15 suppressed miR‐502‐5p expression, and miR‐502‐5p inhibited HMGB3 expression. Low miR‐502‐5p expression was associated with unfavorable outcomes in bladder cancer patients. miR‐502‐5p silencing and HMGB3 overexpression counteracted the inhibition of circTAF15 knockdown on the malignant phenotype of bladder cancer cells. circTAF15 knockdown attenuated the in vivo growth of bladder cancer cells. circTAF15 enhanced the progression of bladder cancer through upregulating HMGB3 via suppressing miR‐502‐5p. circTAF15 may be a novel target to treat bladder cancer in the future.