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

Autor:	Pernot S; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France., Tomé M; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France., Galeano-Otero I; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France., Evrard S; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France., Badiola I; Department of Cell Biology and Histology, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain., Delom F; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France., Fessart D; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France., Smani T; Group of Cardiovascular Pathophysiology, Institute of Biomedicine of Seville, University Hospital of Virgen del Rocío/University of Seville/CSIC, Seville, Spain., Siegfried G; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France., Villoutreix BO; Integrative Computational Pharmacology and Data Mining, INSERM UMR 1141, Rob-ert-Debré Hospital, Paris, France., Khatib AM; Reprograming tumor activitY and associaTed MicroenvironmEnt (Rytme), Bordeaux Institute of Oncology (BRIC)-UMR1312 Inserm, Université of Bordeaux, Pessac, France.; Institut Bergonié, Bordeaux, France.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2024 Jan 05; Vol. 14, pp. 1278630. Date of Electronic Publication: 2024 Jan 05 (Print Publication: 2023).
DOI:	10.3389/fimmu.2023.1278630
Abstrakt:	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. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Pernot, Tomé, Galeano-Otero, Evrard, Badiola, Delom, Fessart, Smani, Siegfried, Villoutreix and Khatib.)
Databáze:	MEDLINE
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