The circACC1/miR-29c-3p/FOXP1 network plays a key role in gastric cancer by regulating cell proliferation.

ABSTRACT

Although substantial progress has been made in early detection and treatment of GC, this disease remains a major burden worldwide. CircRNAs have potential as prognostic and diagnostic biomarkers in tumorigenesis. Therefore, we aimed to clarify the role and mechanism of circACC1 in GC cell proliferation. The expression levels of circACC1, miR-29c-3p and FOXP1 were validated in GC tissue samples and adjacent tissue samples. The impact of circACC1 and miR-29c-3p on overall survival was evaluated in GC specimens. A functional study was performed on MKN-45 and BGC823 cells transfected with different vectors. Cell proliferation was assayed by CCK-8 and colony formation assays. The interactions among circACC1, miR-29c-3p and FOXP1 were tested by RNA immunoprecipitation and luciferase reporter assays. This study demonstrated that circACC1 is upregulated in GC tissues, and its upregulation predicts poorer OS in GC patients. Upregulation of circACC1 promoted GC cell proliferation, as indicated by CCK-8 and colony formation assays. A mechanistic study revealed that the pro-oncogenic effect of circACC1 was mainly caused by binding to miR-29c-3p, thus regulating expression of its downstream target FOXP1. The circACC1/miR-29c-3p/FOXP1 network plays a key role in gastric cancer by regulating cell proliferation.