ArticleJournal of Cancer2025
Dasatinib inhibits PD-L1 expression via a proteasomal pathway in pancreatic ductal adenocarcinoma cells.
Article in Journal of Cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a 5-year survival rate of below 8%. Standard chemotherapy regimens, including gemcitabine and FOLFIRINOX (fluorouracil, leucovorin, irinotecan, and oxaliplatin), offer limited clinical benefits. Although immune checkpoint inhibitors (ICIs) have revolutionized cancer immunotherapy, PDAC remains largely unresponsive to ICI monotherapy. In this study, we demonstrate that dasatinib, a multi-targeted tyrosine kinase inhibitor, reduces programmed death ligand 1 (PD-L1) expression in PDAC cells via a proteasome-dependent degradation pathway. Moreover, PD-L1 levels were correlated with dasatinib sensitivity, suggesting its utility as a predictive biomarker. These findings not only elucidate a novel mechanism of dasatinib's action but also provide a strong rationale for combining dasatinib with ICIs to overcome immune resistance and enhance therapeutic efficacy against PDAC.
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