دورية أكاديمية

Sulconazole inhibits PD-1 expression in immune cells and cancer cells malignant phenotype through NF-κB and calcium activity repression

التفاصيل البيبلوغرافية
العنوان: Sulconazole inhibits PD-1 expression in immune cells and cancer cells malignant phenotype through NF-κB and calcium activity repression
المؤلفون: Simon Pernot, Mercedes Tomé, Isabel Galeano-Otero, Serge Evrard, Iker Badiola, Frederic Delom, Delphine Fessart, Tarik Smani, Geraldine Siegfried, Bruno O. Villoutreix, Abdel-Majid Khatib
المصدر: Frontiers in Immunology, Vol 14 (2024)
بيانات النشر: Frontiers Media S.A., 2024.
سنة النشر: 2024
المجموعة: LCC:Immunologic diseases. Allergy
مصطلحات موضوعية: PD-1, Jurkat T cells, PBMCs, NF-κB, calcium, cancer, Immunologic diseases. Allergy, RC581-607
الوصف: The overexpression of the immunoinhibitory receptor programmed death-1 (PD1) on T-cells is involved in immune evasion in cancer. The use of anti-PD-1/PDL-1 strategy has deeply changed the therapies of cancers and patient survival. However, their efficacy diverges greatly along with tumor type and patient populations. Thereby, novel treatments are needed to interfere with the anti-tumoral immune responses and propose an adjunct therapy. In the current study, we found that the antifungal drug Sulconazole (SCZ) inhibits PD-1 expression on activated PBMCs and T cells at the RNA and protein levels. SCZ repressed NF-κB and calcium signaling, both, involved in the induction of PD-1. Further analysis revealed cancer cells treatment with SCZ inhibited their proliferation, and migration and ability to mediate tumor growth in zebrafish embryos. SCZ found also to inhibit calcium mobilization in cancer cells. These results suggest the SCZ therapeutic potential used alone or as adjunct strategy to prevent T-cell exhaustion and promotes cancer cell malignant phenotype repression in order to improve tumor eradication.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1664-3224
03445089
Relation: https://www.frontiersin.org/articles/10.3389/fimmu.2023.1278630/full; https://doaj.org/toc/1664-3224
DOI: 10.3389/fimmu.2023.1278630
URL الوصول: https://doaj.org/article/90571bd8e03445089bd4c69afb1017e6
رقم الأكسشن: edsdoj.90571bd8e03445089bd4c69afb1017e6
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16643224
03445089
DOI:10.3389/fimmu.2023.1278630