ArticleBlood advances2022
Bone marrow stroma cells promote induction of a chemoresistant and prognostic unfavorable S100A8/A9high AML cell subset.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
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- Multiomic State-Transitions Reveal Post-Treatment Transcriptome Desynchronization in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026Article
- Targeting mitochondrial calcium homeostasis via novel S100A9 inhibitor B2 as a promising agent against AML.Journal of translational medicine · 2026Article
- Succinate receptor 1 restricts hematopoiesis and prevents acute myeloid leukemia progression.Nature communications · 2026Article
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- CD69 predicts prognosis through immune cell infiltration and decitabine treatment response in acute myeloid leukemia.Translational cancer research · 2025Article
- S100P is a core gene for diagnosing and predicting the prognosis of sepsis.Scientific reports · 2025Article
- An integrative multiparametric approach stratifies putative distinct phenotypes of blast phase chronic myelomonocytic leukemia.Cell reports. Medicine · 2025Article
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- GANT61 surmounts drug resistance of ADR by upregulating lysosome activities and reducing BCL2 expression in HL-60/ADR cells.Cancer cell international · 2024Article
- Instructive interaction between myelodysplastic hematopoiesis and the bone marrow microenvironment at the single-cell level.Blood neoplasia · 2024Article
- Identification of two key biomarkers CD93 and FGL2 associated with survival of acute myeloid leukaemia by weighted gene co-expression network analysis.Journal of cellular and molecular medicine · 2024Article
- Application of omics in the diagnosis, prognosis, and treatment of acute myeloid leukemia.Biomarker research · 2024Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bone marrow (BM) stroma represents a protective niche for acute myeloid leukemia (AML) cells. However, the complex underlying mechanisms remain to be fully elucidated. We found 2 small, intracellular, calcium-sensing molecules, S100A8 and S100A9, among the top genes being upregulated in primary AML blasts upon stromal contact. As members of the S100 protein family, they can modulate such cellular processes as proliferation, migration, and differentiation. Dysregulation of S100 proteins is described as a predictor of poor survival in different human cancers, including increased S100A8 expression in de novo AML. Thus, we wanted to decipher the underlying pathways of stroma-mediated S100A8/A9 induction, as well as its functional consequences. Upregulation of S100A8/A9 after stromal cross talk was validated in AML cell lines, was contact independent and reversible and resulted in accumulation of S100A8/A9high cells. Accordingly, frequency of S100A8/A9high AML blasts was higher in the patients' BM than in peripheral blood. The S100A8/A9high AML cell population displayed enhanced utilization of free fatty acids, features of a more mature myeloid phenotype, and increased resilience toward chemotherapeutics and BCL2 inhibition. We identified stromal cell-derived interleukin-6 (IL-6) as the trigger for a Jak/STAT3 signaling-mediated S100A8/A9 induction. Interfering with fatty acid uptake and the IL-6-Jak/STAT3 pathway antagonized formation of S100A8/A9high cells and therapeutic resistance, which could have therapeutic implications as a strategy to interfere with the AML-niche dynamics.
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