ArticleCancer management and research2021
Dl-3-N-Butylphthalide Presents Anti-Cancer Activity in Lung Cancer by Targeting PD-1/PD-L1 Signaling.
Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Histone acetyltransferase HBO1 in cancer biology: Essential mechanisms and implications for targeted therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- The role of histone post-translational modifications in cancer and cancer immunity: functions, mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- Post-translational modifications of histones: Mechanisms, biological functions, and therapeutic targets.MedComm · 2023Review
- Anti-Glioma Effects of Ligustilide or n-Butylphthalide on Their Own and the Synergistic Effects with Temozolomide via PI3K/Akt Signaling Pathway.OncoTargets and therapy · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLung cancer serves as one of the most malignant cancer types. Immunotherapy targeting PD-1/PD-L1 axis is a promising strategy for cancer treatment. Dl-3-N-butylphthalide (NBP), a small molecule compound extracted from the seeds of Apium graveolens, possesses a large range of biological effects and demonstrates anti-cancer activities. However, the role of NBP in the modulation of lung cancer remains obscure.
methodsIn this study, we aimed to explore the effect of NBP on PD-L1 signaling and the progression of lung cancer.
resultsSignificantly, the treatment of NBP repressed the proliferation of lung cancer cells in vitro. Tumorigenicity analysis in nude mice showed that the tumor volume and tumor weight were attenuated by the treatment of NBP in the mice. Meanwhile, the levels of Ki-67 and PD-L1 were reduced by the treatment of NBP in the tumor tissues of the mice. NBP suppressed IFN-γ-induced PD-L1 enhancement in lung cancer cells. The treatment of NBP inhibited PD-L1 expression in lung cancer cells co-cultured with unstimulated PBMCs or activated T cell. NBP inhibited PD-1 expression in activated T cells co-cultured with lung cancer cells. Conditioned medium from activated T cells increased PD-L1 expression, and NBP reversed this effect. Co-culture with A549 and H1975 cells reduced T cell proliferation and activity, while the treatment of NBP reversed the reduction. Consistently, the treatment of NBP caused notably decreased apoptosis of co-cultured T cells. Mechanically, KAT7 was able to bind to PD-L1 promoter and epigenetically induce PD-L1 expression by promoting the enrichment of histone H3 lysine 14 acetylation (H3K14ac) and RNA polymerase II on PD-L1 promoter. DISCUSSION: Thus, we concluded that NBP repressed PD-L1 expression by targeting KAT7 and attenuated PD-1/PD-L1 axis to relieve lung cancer progression. NBP may be applied as the potential therapeutic strategy in immunotherapy of lung cancer.
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