Aberrant expression of circular RNAs (circRNAs) is important in carcinogenesis, however, many differentially expressed circRNAs have not been functionally characterized. This study aimed to unveil the role of circRNA-dual specificity phosphatase 22 (circDUSP22) in pancreatic cancer (PaCa). Expression analyses of circDUSP22, miR-1178-3p and BCL2 interacting protein 3 (BNIP3) were carried out using quantitative real-time PCR (qRT-PCR) or western blotting. Cell growth was assessed by MTT, EdU and colony formation assays. Cell cycle distribution and cell apoptosis were investigated using flow cytometry assay. The assumed binding relationship between miR-1178-3p and circDUSP22 or BNIP3 was testified by dual-luciferase reporter and pull-down assays. The effect of circDUSP22 in vivo was identified by animal studies. The decreased expression of circDUSP22 was observed in PaCa samples and cells. CircDUSP22 ectopic expression in vitro blocked PaCa cell proliferation, arrested cell cycle and provoked cell apoptosis. CircDUSP22 targeted miR-1178-3p, whose expression was reinforced in PaCa. The inhibitory cell growth caused by circDUSP22 ectopic expression was reversed by miR-1178-3p enrichment. In addition, miR-1178-3p targeted BNIP3, whose expression was declined in PaCa. The inhibitory cell growth caused by circDUSP22 ectopic expression was reversed by BNIP3 knockdown. CircDUSP22 overexpression in vivo decelerated tumor growth. CircDUSP22 upregulation blocked PaCa development partly by targeting miR-1178-3p and increasing BNIP3, implying the potential implication of circDUSP22 in targeted therapy of PaCa.

环状RNA (circRNA) 的异常表达在致癌过程中很重要，然而，许多差异表达的circRNA 尚未得到功能表征。本研究旨在揭示 circRNA-双特异性磷酸酶 22 (circDUSP22) 在胰腺癌 (PaCa) 中的作用。使用定量实时 PCR (qRT-PCR) 或蛋白质印迹法对 ​​circDUSP22、miR-1178-3p 和 BCL2 相互作用蛋白 3 (BNIP3) 进行表达分析。通过 MTT、EdU 和集落形成测定评估细胞生长。使用流式细胞术测定细胞周期分布和细胞凋亡。 miR-1178-3p 和 circDUSP22 或 BNIP3 之间假定的结合关系通过双荧光素酶报告基因和 Pull-down 测定进行了验证。通过动物研究鉴定了 circDUSP22 的体内作用。在 PaCa 样品和细胞中观察到 circDUSP22 表达降低。 CircDUSP22 体外异位表达可阻断 PaCa 细胞增殖、阻滞细胞周期并引发细胞凋亡。 CircDUSP22 靶向 miR-1178-3p，其表达在 PaCa 中得到增强。 miR-1178-3p 富集可逆转由 circDUSP22 异位表达引起的抑制性细胞生长。此外，miR-1178-3p 靶向 BNIP3，其表达在 PaCa 中下降。 BNIP3 敲低可逆转由 circDUSP22 异位表达引起的抑制性细胞生长。 CircDUSP22 体内过度表达可减缓肿瘤生长。 CircDUSP22 上调部分通过靶向 miR-1178-3p 和增加 BNIP3 阻断 PaCa 发育，这意味着 circDUSP22 在 PaCa 靶向治疗中的潜在意义。