Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies and 
is known for its high resistance and low response to treatment. Tumor immune 
evasion is a major stumbling block in designing effective anticancer therapeutic 
strategies. Karyopherin alpha 2 (KPNA2), a member of the nuclear transporter 
family, is elevated in multiple human cancers and accelerates carcinogenesis. 
However, the specific role of KPNA2 in PDAC remains unclear. In this study, we 
found that expression of KPNA2 was significantly upregulated in PDAC compared to 
adjacent nontumor tissue and its high expression was correlated with poor 
survival outcome by analyzing the GEO datasets. Similar KPNA2 expression pattern 
was also found in both human patient samples and KPC mouse models through IHC 
staining. Although KPNA2 knockdown failed to impair the vitality and migration 
ability of PDAC cells in vitro, the in vivo tumor growth was significantly 
impeded and the expression of immune checkpoint ligand PD-L1 was reduced by 
silencing KPNA2. Furthermore, we uncovered that KPNA2 modulated the expression 
of PD-L1 by mediating nuclear translocation of STAT3. Collectively, our data 
suggested that KPNA2 has the potential to serve as a promising biomarker for 
diagnosis in PDAC.