Background
Much effort is underway to elucidate the molecular basis of gastric cancer (GC) and to identify predictive biomarkers. circRNAs represent the new non-coding RNAs (ncRNAs) that show abnormal expression within diverse cancers, such as GC. circSTRBP, for instance, is suggested to show overexpression within GC cells and tissues; however, the specific functions of this circSTRBP in cancer progression and the mechanisms involved have not been investigated.
Methods
circSTRBP levels within GC cells and tissues were measured by RT-qPCR. The stability of circSTRBP was assessed by actinomycin D and Ribonuclease R treatments. Cell proliferation, migration, invasion, and angiogenesis after knockdown of exosomal circSTRBP were analyzed through CCK-8 assay, transwell culture system, and tube formation assay. The interaction of circSTRBP with the predicted target miRNAs, miR-1294, miR-593-3p was evaluated by RNA immunoprecipitation chip and luciferase reporter assays. E2F2 expression was determined by western blot analysis. Moreover, this work established the xenograft tumor model for determining in vivo expression and functions of exosomal circSTRBP in gastric cancer.
Results
circSTRBP was upregulated in gastric cancer cells and tissues, and increased within GC cells-derived exosomes. circSTRBP in exosomes enhanced GC cell growth and migration in vitro, which could affect GC development through modulating E2F2 activity. Additionally, in a GC xenograft mouse model, exosomal circSTRBP was shown to promote tumor growth.
Conclusion
Exosomal circSTRBP shows critical biological effects and can modulate key pathways related to gastric cancer progression.
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