Arsenic sulfide inhibits the progression of gastric cancer through regulating the circRNA_ASAP2/Wnt/β-catenin pathway

In our paper, the effects of As(4)S(4) treatments on the growth and migration of gastric cancer (GC) cells were explored, and the potential underlying molecular mechanisms were also identified. Cell viability was evaluated by cell counting kit 8 assay. The expression of Ki-67 was examined using immunofluorescence staining. Cell apoptosis was assessed by flow cytometry. The migratory and invasion abilities of cells were determined using Transwell assay. The mRNA and protein levels of related gene were examined by RT-qPCR and western blotting, respectively. CircRNAs chip was performed to identify the differentiated expression of circRNAs in GC cells following the treatment with As(4)S(4). Our results revealed that the proliferation, migration and invasion of GC cells were remarkably suppressed by the treatment with As(4)S(4), while cell apoptosis was promoted. Furthermore, circRNA_ASAP2 was a novel target of As(4)S(4) in GC, and it is involved in As(4)S(4)-modulated biological behavior alterations in GC cells. In addition, the activities of the Wnt/β-catenin signaling in GC cells were affected by the overexpression circRNA_ASAP2 and the treatment with As(4)S(4.) Moreover, the behavior changes in GC cells caused by the knockdown of circRNA_ASAP2 were reversed by the treatment with Wnt agonist SKL2001. In summary, As(4)S(4) could function as an antitumor agent in GC through regulating the circRNA_ASAP2/Wnt/β-catenin pathway, which in turn influences the growth and metastasis of GC cells.