Emerging evidence indicates the critical roles of N⁶-methyladenosine (m⁶A) modification in human cancers. Herein, our work reported that a novel m⁶A-modified circRNA from the MYO1C gene, circMYO1C, upregulated in the pancreatic ductal adenocarcinoma (PDAC). Our findings demonstrated that circMYO1C is highly expressed in PDAC tissues. Functionally, circMYO1C promoted the proliferation and migration of PDAC cells in vitro and its silencing reduced the tumor growth in vivo. Mechanistically, circMYO1C cyclization was mediated by m⁶A methyltransferase METTL3. Moreover, methylated RNA immunoprecipitation sequencing (MeRIP-seq) unveiled the remarkable m⁶A modification on PD-L1 mRNA. Moreover, circMYO1C targeted the m⁶A site of PD-L1 mRNA to enhance its stability by cooperating with IGF2BP2, thereby accelerating PDAC immune escape. In conclusion, these findings highlight the oncogenic role of METTL3-induced circMYO1C in PDAC tumorigenesis via an m⁶A-dependent manner, inspiring a novel strategy to explore PDAC epigenetic therapy.