circFIG 4 drives the carcinogenesis and metastasis of esophagus cancer via the miR‐493‐5p/E2F3 axis

BACKGROUND: Esophageal cancer (EC) is a highly malignant tumor of the digestive tract. Circular RNAs (circRNAs) have been verified to play a regulatory role in the occurrence and progression of different cancers, including EC. This research aimed to investigate the role and molecular mechanism of circFIG 4 in EC progression. METHODS: The analyses of circFIG 4, miR‐493‐5p, and neuro‐oncological ventral antigen 2 levels were administrated by quantitative real‐time polymerase chain reaction. The characteristics of circFIG 4 were determined by Ribonuclease R assay and Actinomycin D assay. Cell proliferation was assessed via colony formation assay and 5‐ethynyl‐2′‐deoxyuridine incorporation assay. Cell cycle distribution and apoptosis were evaluated by flow cytometry. Western blot was performed to assess protein expression. The targeted interaction among circFIG 4, miR‐493‐5p, and E2F transcription factor 3 (E2F3) were validated using dual‐luciferase reporter or RNA immunoprecipitation assays. RESULTS: circFIG 4 was overtly upregulated in EC and was relatively stable in EC cells. circFIG 4 knockdown impeded proliferation, migration, and invasion and expedited apoptosis in EC cells. circFIG 4 served as a miR‐493‐5p sponge to act in the development of EC. Furthermore, circFIG 4 modulated EC progression via targeting miR‐493‐5p and miR‐493‐5p suppressed EC progression via targeting E2F3. circFIG 4 modulated E2F3 expression through acting as a sponge of miR‐493‐5p. Moreover, circFIG 4 knockdown inhibited EC tumorigenesis by targeting miR‐493‐5p/E2F3 axis tumor growth in vivo. CONCLUSION: circFIG 4 silence mitigated EC malignant progression at least partly by mediating the miR‐493‐5p/E2F3 pathway, highlighting new biomarkers and therapeutic targets for EC treatment.