Hsa_circ_0005050 interacts with ILF3 and affects cell apoptosis and proliferation by disrupting the balance between p53 and p65

The regulatory network between arsenic, genes and signaling pathways has been reported in arsenic carcino-genesis. Studies on circRNA represent a growing field, but the extent to circRNA potential mechanisms remains poorly understood. So this study we explore the systematic function of hsa_circ_0005050 in mediating the cell apoptosis and proliferation. We demonstrated that hsa_circ_0005050 was highly expressed in subjects who are long-term exposed to arsenic, and could be induced by NaAs2O3 in A549 and 16HBE. Knockdown of hsa_-circ_0005050 promotes A549 cell viability, whereas exerts the opposite effects in 16HBE. Mechanistically, hsa_circ_0005050 regulates the p53 and NF -KB signaling pathway involved in the apoptosis and proliferation. And we found that hsa_circ_0005050 could directly bind to the RNA binding protein ILF3 and mutually influence each other's formation. Upon si-hsa_circ_0005050, ILF3 export to the cytoplasm resulting the formation of a ternary complex ILF3-p65-IKBA, breaks the balance of p53 and NF -KB pathway and induces A549 apoptosis and leads to 16HBE proliferation. As a result of these investigations, suggestions were identified for future research.

Automated summary

This study explored the role of hsa_circ_0005050 in mediating cell apoptosis and proliferation. It was found that hsa_circ_0005050 was highly expressed in individuals exposed to arsenic and could regulate the p53 and NF-KB signaling pathways to affect cell survival and proliferation. Additionally, hsa_circ_0005050 was found to interact with the RNA binding protein ILF3, influencing each other's formation.