Combination　chemotherapy　and　immunotherapy　have　failed　to　achieve　breakthroughs　in　pancreatic　ductal　adenocarcinoma　(PDAC).　Chemotherapy-induced　senescence　is　a　potential　solution　for　this　problem.　This　study　integrates　clinical　samples　with　single-cell　transcriptomic　sequencing,　proteomics,　and　RNA　sequencing　and　reveals　that　FOLFIRINOX　(a　combination　regimen　of　5-fluorouracil,　oxaliplatin,　irinotecan,　and　leucovorin)　treatment　induces　a　higher　proportion　of　senescent　tumor　cells　(senTCs).　This　phenomenon　is　principally　attributed　to　the　presence　of　cCCT2,　which　inhibits　SLX4　condensate-mediated　DNA　damage　repair　pathways　by　regulating　small　ubiquitin-like　modifier　conjugation,　thereby　promoting　tumor　cell　senescence.　In　the　tumor　immune　microenvironment,　cCCT2-overexpressing　senTCs　exhibit　a　senescence-associated　secretory　phenotype　(SASP)　with　preferential　secretion　of　CXCL10,　which　induces　chemotaxis　of　CD8(+)　T-cells.　Based　on　the　pro-senescence　and　immune-microenvironment-remodeling　effects　of　cCCT2,　an　engineered　exosome-loaded　circRNA　system,　SenExo-cCCT2　is　developed.　When　combined　with　SenExo-cCCT2,　the　FOLFIRINOX　regimen　enhances　the　capacity　of　pancreatic　cancer　cells　to　induce　senescence.　Subsequently,　anti-PD-L1　therapy　facilitates　the　immune-mediated　clearance　of　senTCs,　markedly　improving　the　therapeutic　efficacy　of　combined　chemotherapy　and　immunotherapy　for　pancreatic　cancer.