Inflammatory signaling pathways play a role in SYK inhibitor resistant AML

Abstract Trials have shown promising clinical activity of the selective SYK inhibitor entospletinib in patients with high expressing HOXA9/MEIS1 acute leukemias. As the development of resistance mechanisms is a common problem in the use of targeted drugs, we performed a chemical library screen to id...

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Main Authors: Sarah Tausch, Christina Villinger, Gabriela Alexe, Daniel J. Urban, Min Shen, Dominique Jahn, Jonas Vischedyk, Sebastian Scheich, Hubert Serve, Matthew D. Hall, Kimberly Stegmaier, Thomas Oellerich, Anjali Cremer
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Language:English
Published: Nature Portfolio 2025-04-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-96660-w
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author Sarah Tausch
Christina Villinger
Gabriela Alexe
Daniel J. Urban
Min Shen
Dominique Jahn
Jonas Vischedyk
Sebastian Scheich
Hubert Serve
Matthew D. Hall
Kimberly Stegmaier
Thomas Oellerich
Anjali Cremer
author_facet Sarah Tausch
Christina Villinger
Gabriela Alexe
Daniel J. Urban
Min Shen
Dominique Jahn
Jonas Vischedyk
Sebastian Scheich
Hubert Serve
Matthew D. Hall
Kimberly Stegmaier
Thomas Oellerich
Anjali Cremer
author_sort Sarah Tausch
collection DOAJ
description Abstract Trials have shown promising clinical activity of the selective SYK inhibitor entospletinib in patients with high expressing HOXA9/MEIS1 acute leukemias. As the development of resistance mechanisms is a common problem in the use of targeted drugs, we performed a chemical library screen to identify drug sensitivities in SYK inhibitor resistant AML cells. We identified that SYK inhibitor resistant cells displayed an increased sensitivity to glucocorticoids. Glucocorticoids are potent immunosuppressants which work in part by inhibiting the transcription of cytokine genes. RNA sequencing of entospletinib resistant cells revealed a strong enrichment of inflammatory response and TNFα signaling via NF-κB gene sets in comparison to naive cells. Naive AML cells treated with entospletinib showed a strong downregulation of the same gene sets which were upregulated in the resistant state. Our data suggest that inflammatory signaling pathways play a role in entospletinib resistant AML cells.
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spelling doaj-art-12f48a8d33da4ab09f09fd148af6232e2025-08-20T03:05:01ZengNature PortfolioScientific Reports2045-23222025-04-0115111110.1038/s41598-025-96660-wInflammatory signaling pathways play a role in SYK inhibitor resistant AMLSarah Tausch0Christina Villinger1Gabriela Alexe2Daniel J. Urban3Min Shen4Dominique Jahn5Jonas Vischedyk6Sebastian Scheich7Hubert Serve8Matthew D. Hall9Kimberly Stegmaier10Thomas Oellerich11Anjali Cremer12Department of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Pediatric Oncology, Harvard Medical School, Dana-Farber Cancer Institute and Boston Children’s HospitalDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of HealthDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of HealthDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDivision of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of HealthDepartment of Pediatric Oncology, Harvard Medical School, Dana-Farber Cancer Institute and Boston Children’s HospitalDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityDepartment of Medicine, Hematology/Oncology, University Hospital Frankfurt, Goethe UniversityAbstract Trials have shown promising clinical activity of the selective SYK inhibitor entospletinib in patients with high expressing HOXA9/MEIS1 acute leukemias. As the development of resistance mechanisms is a common problem in the use of targeted drugs, we performed a chemical library screen to identify drug sensitivities in SYK inhibitor resistant AML cells. We identified that SYK inhibitor resistant cells displayed an increased sensitivity to glucocorticoids. Glucocorticoids are potent immunosuppressants which work in part by inhibiting the transcription of cytokine genes. RNA sequencing of entospletinib resistant cells revealed a strong enrichment of inflammatory response and TNFα signaling via NF-κB gene sets in comparison to naive cells. Naive AML cells treated with entospletinib showed a strong downregulation of the same gene sets which were upregulated in the resistant state. Our data suggest that inflammatory signaling pathways play a role in entospletinib resistant AML cells.https://doi.org/10.1038/s41598-025-96660-wAcute myeloid leukemia cellsResistanceInflammatory pathwaysGlucocorticoids
spellingShingle Sarah Tausch
Christina Villinger
Gabriela Alexe
Daniel J. Urban
Min Shen
Dominique Jahn
Jonas Vischedyk
Sebastian Scheich
Hubert Serve
Matthew D. Hall
Kimberly Stegmaier
Thomas Oellerich
Anjali Cremer
Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
Scientific Reports
Acute myeloid leukemia cells
Resistance
Inflammatory pathways
Glucocorticoids
title Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
title_full Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
title_fullStr Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
title_full_unstemmed Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
title_short Inflammatory signaling pathways play a role in SYK inhibitor resistant AML
title_sort inflammatory signaling pathways play a role in syk inhibitor resistant aml
topic Acute myeloid leukemia cells
Resistance
Inflammatory pathways
Glucocorticoids
url https://doi.org/10.1038/s41598-025-96660-w
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