ArticleBlood cancer journal2023
Targeting S100A9 protein affects mTOR-ER stress signaling and increases venetoclax sensitivity in Acute Myeloid Leukemia.
Article in Blood cancer journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 15 citations in OpenAlex.
- A Nutrient-Sensitive ZRF1-Dependent Secretory Network Involving S100A9 Contributes to Neutrophil Plasticity in Triple-Negative Breast Cancer.ACS pharmacology & translational science · 2026Article
- Mesenchymal stem cell-induced metabolic reprogramming of EGFR-wild-type tumor cells drives therapeutic resistance in EGFR-mutant non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Article
- Targeting mitochondrial calcium homeostasis via novel S100A9 inhibitor B2 as a promising agent against AML.Journal of translational medicine · 2026Article
- Exosomal S100A9 promotes lung metastasis of adenoid cystic carcinoma via activating cancer-associated fibroblasts.Cell death discovery · 2026Article
- Phytochemicals as potential inhibitors of NETosis: implications for immunothrombosis and chronic disease management.BMC complementary medicine and therapies · 2026Article
- Article
- Integrated bulk and single-cell transcriptomics identify RELB, S100A9, and SOCS1 as key autophagy-endoplasmic reticulum stress genes linking T2DM with MAFLD.Scientific reports · 2025Article
- Targeting S100A9-mediated inflammation: a novel therapeutic approach for CLL.Blood advances · 2025Review
- S100A9 promotes resistance to anti-PD-1 immunotherapy in hepatocellular carcinoma by degrading PARP1 and activating the STAT3/PD-L1 pathway.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Talazoparib and radiation enhance the senolytic efficacy of venetoclax in therapy-induced senescent triple-negative breast cancer cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Article
- Inhibiting the alarmin-driven hematopoiesis-stromal cell crosstalk in primary myelofibrosis ameliorates bone marrow fibrosis.HemaSphere · 2025Article
- Non-essential role of S100A9 in hematopoiesis in primary MPN and MDS mouse models.Cancer biology & medicine · 2025Article
- Endoplasmic Reticulum Stress in Acute Myeloid Leukemia: Pathogenesis, Prognostic Implications, and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- S100A10 knockdown exacerbates phenylephrine-induced cardiomyocyte hypertrophy via modulating mitochondrial oxidative phosphorylation.Frontiers in genetics · 2025Article
- The role of calprotectin in giant cell arteritis - from pathophysiology to possible clinical applications.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
Acute Myeloid Leukemia (AML) is a heterogeneous disease with limited treatment options and a high demand for novel targeted therapies. Since myeloid-related protein S100A9 is abundantly expressed in AML, we aimed to unravel the therapeutic impact and underlying mechanisms of targeting both intracellular and extracellular S100A9 protein in AML cell lines and primary patient samples. S100A9 silencing in AML cell lines resulted in increased apoptosis and reduced AML cell viability and proliferation. These therapeutic effects were associated with a decrease in mTOR and endoplasmic reticulum stress signaling. Comparable results on AML cell proliferation and mTOR signaling could be observed using the clinically available S100A9 inhibitor tasquinimod. Interestingly, while siRNA-mediated targeting of S100A9 affected both extracellular acidification and mitochondrial metabolism, tasquinimod only affected the mitochondrial function of AML cells. Finally, we found that S100A9-targeting approaches could significantly increase venetoclax sensitivity in AML cells, which was associated with a downregulation of BCL-2 and c-MYC in the combination group compared to single agent therapy. This study identifies S100A9 as a novel molecular target to treat AML and supports the therapeutic evaluation of tasquinimod in venetoclax-based regimens for AML patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.