Hsa_circ_0030586 promotes epithelial–mesenchymal transition in prostate cancer via PI3K-AKT signaling

Abstract

ABSTRACT Circular RNAs (CircRNAs) gain importance as regulatory molecules in prostate cancer (PCa), but molecular mechanism of most circRNAs in pathogenesis of PCa remains to be studied. This study aimed to explore the role of hsa_circ_0030586 in PCa. Gene Expression Omnibus database (GSE77661) was used to screen out candidate circRNAs. Quantitative real-time PCR was used to verify the relative expressions of circRNAs, miRNAs, and genes in PCa cells. A CCK-8 assay was used to evaluate the cells’ proliferation. Transwell and wound healing assay were used to determine the cells’ migration and invasion. Western blotting and immunohistochemistry were used to detect the protein expression of PI3K/AKT signaling proteins and epithelial–mesenchymal transition (EMT) markers. Furthermore, a nude mice tumorigenesis experiment in vivo was conducted to determine the function of hsa_circ_0030586 on PCa. Our results showed that hsa_circ_0030586 is significantly upregulated in PCa cells (p < 0.05). Its circular structure was confirmed via agarose gel electrophoresis and Sanger sequencing. Interfering with hsa_circ_0030586 in PC3 cells inhibited cell proliferation, migration, and invasion and led to the significant upregulation of E-cadherin and the significant downregulation of p-AKT/AKT, IKKα, PIK3CB, and Twist (all p < 0.05). Conversely, the hsa_circ_003058 interference fragment combined with the transfection of a miR-145-3p inhibitor could reverse the above effects. In vivo tumorigenesis of the xenograft model confirmed that interfering with hsa_circ_0030586 suppressed tumor cell proliferation and inhibited PI3K-AKT signaling and EMT in PC3 cells. Hsa_circ_0030586 is significantly upregulated in PCa cells and may promote EMT via PI3K-AKT signaling.