Circular RNAs (
circRNAs) have recently emerged as essential regulators in
carcinogenesis and
cancer progression. Previous studies have shown that Cdr1as functions as a
microRNA (
miRNA) sponge in various
cancer types. However, the role of Cdr1as in
cisplatin chemosensitivity in
bladder cancer remains unclear. Here, we used real-time PCR to examine
miRNA and gene expression in
bladder cancer tissues and cell lines. The abilities of Cdr1as and its downstream regulatory molecules to induce apoptosis and promote
cisplatin-induced chemosensitivity of
bladder cancer cells were determined by flow cytometry and cell counting kit. Bioinformatic analysis was utilized to predict potential
miRNA target sites, and
biotin-coupled
miRNA capture,
biotin-coupled probe pull-down assay, and
RNA fluorescent in situ hybridization were used to study the interaction between Cdr1as and target
miRNAs. Dual-
luciferase reporter assay was also used to validate the target genes of
miRNAs. The expression level of
apoptotic protease-activating factor 1 (APAF1) in
bladder cancer cells was identified via western blot. Finally, the sensitivity of Cdr1as to
cisplatin chemotherapy in nude mice xenografts was evaluated in terms of the size, volume of
tumors, and the survival of mice. We report that Cdr1as induced the apoptosis and enhanced the
cisplatin chemosensitivity of
bladder cancer cells both in vitro and in vivo. Silencing of APAF1 reduced the sensitivity of
bladder cancer cells to
cisplatin chemotherapy. Furthermore, Cdr1as could directly sponge miR-1270 and abolish its effect on APAF1. Our study verified that Cdr1as exerts a
cisplatin-chemosensitization effect on
bladder cancer cells through the Cdr1as/miR-1270/APAF1 axis. This newly identified axis may be a potential therapeutic target for
bladder cancer patients.