Abstract
BACKGROUND: Colorectal cancer (CRC) represents a significant global health burden, requiring a deeper understanding of the molecular mechanisms that drive its progression. Circular RNAs (circRNAs) have appeared as crucial regulators in cancer, with circ_0050102 as a potential functional molecule in CRC. The present study aimed to determine the diagnostic and functional implications of circ_0050102 in CRC pathogenesis. METHODS: The GSE172229, GSE205094, and GSE134834 datasets were used for the comprehensive analyses of circRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) in CRC tumor samples. Functional experiments, including fluorescence in situ hybridization, knockdown assays, flow cytometric analysis, and luciferase reporter assay, were conducted to investigate the effect of circ_0050102 on CRC cell behavior. CircRNA - miRNA - mRNA interaction analysis provided information about the regulatory network that involved circ_0050102, miR-3622a-3p, and baculoviral IAP repeat-containing 5 (BIRC5). Furthermore, the functional impact of circ_0050102 on CRC tumor growth was investigated using in vivo xenograft models. RESULTS: Our analysis determined circ_0050102 as a significantly differentially expressed circRNA in CRC, with a high area under the receiver operating characteristic curve value, indicating its diagnostic potential. Functional experiments revealed that circ_0050102 is predominantly localized in the cytoplasm of CRC tumor cells, and its knockdown significantly attenuates various CRC cell behavior aspects, including viability, invasion, and migration (p < 0.05). The interaction analysis revealed a potential regulatory axis that involves circ_0050102, miR-3622a-3p, and BIRC5. In vivo experiments demonstrated that circ_0050102 knockdown significantly attenuated CRC tumor development. CONCLUSION: Our results revealed that circ_0050102 promotes CRC progression through miR-3622a-3p and BIRC5. The circ_0050102-mediated regulatory network provides valuable information about the intricate mechanisms contributing to CRC pathogenesis.