Background Circular RNAs (circRNAs) represent a distinct class of non-coding RNAs that have attracted substantial research attention in recent years. We identified a novel circRNA derived from golgi glycoprotein 1… Click to show full abstract
Background Circular RNAs (circRNAs) represent a distinct class of non-coding RNAs that have attracted substantial research attention in recent years. We identified a novel circRNA derived from golgi glycoprotein 1 mRNA (circ_GLG1), the role of which is unknown in colorectal cancer (CRC). The purpose of this study was to explore the potential roles and mechanisms of circ_GLG1 in CRC. Materials and Methods Quantitative reverse transcriptase-polymerase chain reaction analysis was performed to quantify circ_GLG1 expression in 40 pairs of CRC tissues and adjacent normal tissues as well as CRC cell lines. DLD1 CRC cells were transfected with a small-interfering RNA against circ_GLG1, after which cell proliferation, viability, invasion, and migration were measured through cell counting kit-8 colony-formation, transwell, and wound-healing assays, respectively. Dual-luciferase reporter assays were performed to explore the binding sites among circ_GLG1, miR-622, and Kirsten rat sarcoma (KRAS) transcripts. KRAS protein expression was detected using Western blot analysis. Results Circ_GLG1 expression was significantly higher in CRC tissues than in adjacent normal tissues. Knocking down circ_GLG1 in DLD1 cells inhibited tumor cell viability, proliferation, invasion, and migration, and these effects were reversed by co-transfecting an miR-622 inhibitor. Circ_GLG1 promoted KRAS expression at both the mRNA and protein levels by acting as an miR-622 sponge. Dual-luciferase reporter assays demonstrated that miR-622 interacted with circ_GLG1 and KRAS mRNA. Conclusion Our study revealed the role of the circ_GLG1–miR-622–KRAS axis in CRC. Moreover, our findings provide insight into the molecular mechanism of circ_GLG1 in CRC and suggest potential new biomarkers for diagnosing this disease.
               
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