circATAD2 mitigates CD8+ T cells antitumor immune surveillance in breast cancer via IGF2BP3/m6A/PD-L1 manner

Immune surveillance and chemotherapy sensitivity play critical functions in the tumorigenesis of breast cancer (BC). Emerging findings have indicated that circular RNA (circRNA) and N-6-methyladenosine (m6A) both participate in the BC tumorigenesis. Here, present study aimed to investigate the roles of m(6)A-modified circATAD2 on BC and explore better understanding for BC precision therapeutic. Results reported that m(6)A-modifid circRNA (m(6)A-circRNA) microarray revealed the m(6)A-circRNA landscape in BC. M(6)A-modifid circATAD2 upregulated in BC samples and was closely correlated to poor prognosis. Functionally, circATAD2 promoted the immune evasion of BC cells and reduced the CD8(+) T cells' killing effect. Mechanistically, MeRIP-seq unveiled the m(6)A modification in the 3'-UTR of PD-L1 mRNA, which was bound by circATAD2 and recognized by m(6)A reader IGF2BP3 to enhance PD-L1 mRNA stability and expression. In summary, these findings revealed the circATAD2/m(6)A/IGF2BP3/PD-L1 axis in BC immune surveillance, suggesting the potential that circATAD2 as a potential target for PD-L1-mediated BC.