CircFLNA facilitates gastric cancer cell proliferation and glycolysis via regulating SOX5 by sponging miR-1200.

Abstract

Background and study aims: Circular RNAs (circRNAs) are important regulators for gastric cancer (GC) progression. Our study aims to investigate the role and mechanism of circFLNA in GC progression.

Patients and methods: The levels of circFLNA, microRNA (miR)-1200 and SRY-box transcription factor 5 (SOX5) were examined using qRT-PCR. Flow cytometry, cell counting kit 8 assay and EdU assay were performed to measure cell proliferation and apoptosis. Cell glycolysis ability was assessed by examining glucose uptake and lactate produce. RNA interaction was determined using RNA pull-down assay and dual-luciferase reporter assay. Mice xenograft models were constructed to evaluate the regulation of circFLNA knockdown on GC tumor growth.

Results: CircFLNA was upregulated in GC tissues. Functional experiments showed that circFLNA knockdown suppressed GC cell proliferation, inhibited glycolysis, and promoted apoptosis in vitro, as well as reduced GC tumor growth in vivo. CircFLNA sponged miR-1200, and miR-1200 targeted SOX5. MiR-1200 mimic reversed the promotion effect of circFLNA overexpression on GC cell growth and glycolysis, and SOX5 upregulation also abolished the inhibiting effect of miR-1200 mimic on GC cell growth and glycolysis.

Conclusion: Our data suggest that circFLNA might exert oncogenic role in GC development, which promoted GC proliferation and glycolysis through regulating miR-1200/SOX5 axis.