ArticleCancer management and research2025
Targeting PD-L1 with BMS-202 Enhances Antitumor Cytokine and Cytotoxic T-Lymphocyte Responses in C57BLx/6 Mouse Lung Carcinogenesis.
Article in Cancer management and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Purpose: Lung cancer remains a leading cause of cancer-related mortality, and although immune checkpoint inhibitors have improved outcomes, their use is often limited by immune-related adverse effects and treatment resistance. This study therefore investigates the effects of the small-molecule PD-L1 inhibitor BMS-202 on lung carcinogenesis using a subcutaneous tumor model in C57BL/6 mice. Specifically, we aimed to evaluate its cytotoxic activity, induction of apoptosis, and impact on antitumor immune modulation. Methods: In this study, we utilized in vivo mouse models and in vitro CMT167 cancer cells to evaluate the anti-tumor effects of BMS-202. Tumor growth inhibition was assessed through caliper measurements and histological analysis. Apoptosis was analyzed using AO/PI staining, Annexin V-FITC/PI flow cytometry, Caspase-3 activity assays, and Real-Time PCR to evaluate the expression of apoptosis-related genes (Bad, Bax, Apaf1, Bcl2, and Bcl-xl). Additionally, flow cytometry was employed to analyze lymphocyte infiltration in the tumor microenvironment. Finally, enzyme-linked immunosorbent (ELISA) was used for measurement of cytokines. Results: Specifically, cell viability decreased from 98.1% to 30.1% at concentrations ranging from 0 μM to 40 μM (P<0.001). Apoptosis assays revealed distinct fluorescence patterns indicating increased apoptosis, with late apoptotic cells becoming prominent at higher concentrations. In vivo, results showed that treatment with BMS-202 significantly reduced tumor weight, with mean weights of 609 ± 41.5 mg and 371.88 ± 47.5 mg at 30 mg/kg and 60 mg/kg, respectively (P<0.001). Flow cytometry analysis indicated a marked increase in CD3+CD8+ cytotoxic T cells, rising from 6.8% to 26.2% (P<0.001), and a reduction in PD-1 expression, suggesting enhanced immune activation. Additionally, BMS-202 treatment significantly elevated levels of pro-inflammatory cytokines, including IFN-γ and TNF-α, indicating a robust immune response (P<0.001). Conclusion: These findings suggest that BMS-202 effectively promotes apoptosis and enhances immune responses in lung cancer, underscoring its potential as a therapeutic agent in treating lung carcinogenesis.
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