ArticleEuropean journal of medical research2025
Pirenzepine exhibits anti-prostate cancer activity and enhances checkpoint inhibitor-based immunotherapy by targeting STING.
Article in European journal of medical research, 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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Abstract
purposeTherapeutic options targeting programmed cell death protein 1 (PD-1) and programmed death ligand-1 (PD-L1) have been approved for use in human malignancies, showing clinical benefits. Nonetheless, a significant number of patients, particularly those with prostate cancer (PCa), show poor response to anti-PD-1/PD-L1 therapies, highlighting the necessity to explore supportive strategies that could enhance conventional PD-1/PD-L1-targeting immunotherapy.
methodsPCa cell lines DU145 and RM1 were used to investigate the effects of pirenzepine (PZP) on the proliferation, colony formation, and migration of PCa cells in vitro. A subcutaneous tumor model bearing DU145 and RM1 was established to evaluate the anti-tumor effect in vivo. Lentivirus transfection and quantitative polymerase chain reaction (qPCR) assays were conducted to investigate the role of STING (endoplasmic reticulum-associated protein stimulator of interferon genes) in the antitumor mechanisms of PZP. The infiltration of CD8
resultsThe in vitro and in vivo experiment results indicated that PZP suppressed the proliferation, colony formation, and migration of PCa cells in a dose-dependent manner. Notably, PZP also promoted CD8
conclusionsOur results revealed that PZP impaired the malignant biological behavior of PCa and enhanced antitumor immunity. These findings may provide a theoretical basis for combining PZP with anti-PD1 immune checkpoint blockade therapy on PCa.
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