circMYC promotes cell proliferation, metastasis, and glycolysis in cervical cancer by up-regulating MET and sponging miR-577.

Objective To analyze the role of circMYC in cervical cancer. Methods Protein and RNA expression was detected by RT-qPCR and western blotting. Transwell, CCK8, and colony formation assays were used for measuring metastasis, cell viability, and proliferation, respectively. Lactate production, glucose uptake, and ATP generation were examined to evaluate cell glycolysis. Interactions between circMYC, miR-577, and MET were determined by RNA pull-down and immunoprecipitation, and dual-luciferase reporter assays. Xenografts were established in mice to evaluate the functions of circMYC in vivo. Results circMYC was overexpressed in tumor tissue, which was related to poor prognosis. CircMYC knockdown reduced proliferation, colony formation, metastasis, and glycolysis in cervical cancer cells as well as inhibiting tumor growth in vivo. Mechanistically, circMYC targeted miR-577, and the effects of circMYC knockdown could be reversed by miR-577 inhibition. Moreover, miR-577 downregulated the expression of MET. Therefore, the oncogenic role of circMYC in cervical cancer was achieved by sponging miR-577 and maintaining MET expression. Conclusion circMYC promotes cervical cancer progression through regulation of the miR-577/MET axis. circMYC may thus be a potential target for diagnosing and treating cervical cancer.