Abstract
Recent data indicated that circular RNAs (circRNAs) were implicated in tumor progression including colorectal cancer (CRC). However, the mechanism of hsa_circ_0000467 in CRC remains unclear. The levels of hsa_circ_0000467, microRNA-383-5p (miR-383-5p), and serum/glucocorticoid regulated kinase 1 (SGK1) in CRC tissues and cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability and apoptotic rate were detected through cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The migration and invasion abilities were evaluated via Transwell assay. The protein levels of cleaved caspase 3 (C-caspase 3), B-cell lymphoma 2 (Bcl-2), N-cadherin, E-cadherin, SGK1, and proliferating cell nuclear antigen (PCNA) were detected by western blot assay. The dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were constructed to verify the interaction between miR-383-5p and hsa_circ_0000467 or SGK1. The mouse model experiment was performed to further validate the effects of hsa_circ_0000467 on CRC progression. Hsa_circ_0000467 and SGK1 were enhanced while miR-383-5p was reduced in CRC tissues and cells. Hsa_circ_0000467 silencing suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) but induced apoptosis in CRC cells by regulating miR-383-5p. Hsa_circ_0000467 sponged miR-383-5p and SGK1 was a direct target of miR-383-5p. Besides, hsa_circ_0000467 promoted SGK1 expression in CRC cells by sponging miR-383-5p. Furthermore, miR-383-5p restrained cell proliferation, metastasis, and EMT but facilitated apoptosis in CRC cells by modulating SGK1. Also, hsa_circ_0000467 knockdown blocked xenograft tumor growth in vivo. Hsa_circ_0000467 promoted CRC progression by regulating SGK1 expression via miR-383-5p.