Retracted Article: CircBANP acts as a sponge of let-7a to promote gastric cancer progression via the FZD5/Wnt/β-catenin pathway

Gastric cancer (GC) is one of the leading causes of cancer-related deaths in our country. Circular RNAs (circRNAs) are being found to have relevance to human cancers, including GC. The purpose of this study was to investigate the functional role of circRNA BTG3 associated nuclear protein (circBANP) in GC and underlying mechanisms governing it. CircBANP was identified using RNase R assay and polymerase chain reaction (PCR) with specific primers. The levels of circBANP, let-7a and Frizzled-5 (FZD5) mRNA were assessed by quantitative real-time PCR (qRT-PCR). Cell proliferation, colony formation ability, apoptosis, and migration and invasion were determined by Cell Counting Kit-8 (CCK-8) assay, colony formation assay, flow cytometry, transwell assay, respectively. The targeted interaction between let-7a and circBANP or FZD5 was confirmed by dual-luciferase reporter assay or RNA pull-down assay. Western blot analysis was performed to detect the indicated protein expression. A xenograft model assay was established to observe the role of circBANP in vivo. We found that circBANP was up-regulated in GC tissues and cell lines, and associated with clinicopathologic features of GC patients. CircBANP knockdown repressed the proliferation, migration, invasion, and promoted the apoptosis in GC cells. CircBANP sequestered let-7a by acting as a molecular sponge of let-7a. Moreover, the regulatory effect of circBANP on GC cell progression in vitro was mediated by let-7a. CircBANP protected against FZD5 repression by sponging let-7a in GC cells. Wnt/β-catenin signaling was involved in the regulatory network of the circBANP/let-7a axis in GC cell progression. Additionally, circBANP depletion retarded tumor growth in vivo. In conclusion, our study suggested that the knockdown of circBANP suppressed GC cell progression in vitro and in vivo at least partially through sponging let-7a and regulating FZD5/Wnt/β-catenin signaling, providing a novel mechanism for understanding the pathogenesis of GC.