ArticleOncoimmunology
High mobility group box 1 (HMGB1) acts as an "alarmin" to promote acute myeloid leukaemia progression.
Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Combination of dociparstat sodium (DSTAT), a CXCL12/CXCR4 inhibitor, with azacitidine for the treatment of hypomethylating agent refractory AML and MDS.Leukemia research · 2021Trial
- The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.JCI insight · 2026Review
- TIM-3 in AML: a janus-faced orchestrator of immune exhaustion and leukemic self-renewal.Cancer cell international · 2026Review
- Advances in the study of TIM3 in myelodysplastic syndrome.Frontiers in immunology · 2025Review
- Wuhan strain of SARS-CoV-2 triggers activation of immune evasion machinery similar to the one operated by cancer cells.Frontiers in immunology · 2025Article
- Single-cell transcriptome profiling of mMolecular biomedicine · 2024Article
- The mechanism of high mobility group box-1 protein and its bidirectional regulation in tumors.Biomolecules & biomedicine · 2024Review
- TIM proteins and microRNAs: distinct impact and promising interactions on transplantation immunity.Frontiers in immunology · 2024Review
- Effects of HMGB1/TLR4 on secretion IL-10 and VEGF in human jaw bone-marrow mesenchymal stem cells.Journal of applied oral science : revista FOB · 2024Article
- Mechanisms involved in the HMGB1 modulation of tumor multidrug resistance (Review).International journal of molecular medicine · 2023Article
- Role of innate immunological/inflammatory pathways in myelodysplastic syndromes and AML: a narrative review.Experimental hematology & oncology · 2023Review
- L-Kynurenine participates in cancer immune evasion by downregulating hypoxic signaling in T lymphocytes.Oncoimmunology · 2023Article
- Biologic Functions of Hydroxychloroquine in Disease: From COVID-19 to Cancer.Pharmaceutics · 2022Review
- Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022Review
- TIRAP drives myelosuppression through an Ifnγ-Hmgb1 axis that disrupts the endothelial niche in mice.The Journal of experimental medicine · 2022Article
- Review
- The performance of the alarmin HMGB1 in pediatric diseases: From lab to clinic.Immunity, inflammation and disease · 2021Review
- Chronic stress promotes acute myeloid leukemia progression through HMGB1/NLRP3/IL-1β signaling pathway.Journal of molecular medicine (Berlin, Germany) · 2021Article
- High Mobility Group Box 1 (HMGB1) Induces Toll-Like Receptor 4-Mediated Production of the Immunosuppressive Protein Galectin-9 in Human Cancer Cells.Frontiers in immunology · 2021Article
- HMGB1: an important regulator of myeloid differentiation and acute myeloid leukemia as well as a promising therapeutic target.Journal of molecular medicine (Berlin, Germany) · 2021Article
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1) is a non-histone protein localised in the cell nucleus, where it interacts with DNA and promotes nuclear transcription events. HMGB1 levels are elevated during acute myeloid leukaemia (AML) progression followed by participation of this protein in triggering signalling events in target cells as a pro-inflammatory stimulus. This mechanism was hypothesised to be employed as a survival pathway by malignant blood cells and our aims were therefore to test this hypothesis experimentally. Here we report that HMGB1 triggers the release of tumour necrosis factor alpha (TNF-α) by primary human AML cells. TNF-α induces interleukin 1 beta (IL-1β) production by healthy leukocytes, leading to IL-1β-induced secretion of stem cell factor (SCF) by competent cells (for example endothelial cells). These results were verified in mouse bone marrow and primary human AML blood plasma samples. In addition, HMGB1 was found to induce secretion of angiogenic vascular endothelial growth factor (VEGF) and this process was dependent on the immune receptor Tim-3. We therefore conclude that HMGB1 is critical for AML progression as a ligand of Tim-3 and other immune receptors thus supporting survival/proliferation of AML cells and possibly the process of angiogenesis.
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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.