ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
HMGB1 enhances the protumoral activities of M2 macrophages by a RAGE-dependent mechanism.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 85 citations in OpenAlex.
- Regulatory effects and mechanisms of the acupuncture-induced complement component 1q on the high mobility group box 1 -receptor for advanced glycation end products-nuclear factor kappa-B pathway at Zusanli (ST36).Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications.Cell death discovery · 2026Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Insights into spheroid formation: interaction of ovarian cancer cells with macrophage populations in the tumor microenvironment.Journal of translational medicine · 2025Article
- HMGB1 as an emerging key modulator of bone remodeling: a narrative review.Stem cell research & therapy · 2025Review
- Tumor associated macrophages in gastric cancer dual roles in immune evasion and clinical implications for targeted therapy.Frontiers in immunology · 2025Review
- Single-cell RNA-sequencing analysis of immune and mesenchymal cell crosstalk in the developing enthesis.Scientific reports · 2024Article
- HMGB1 as an extracellular pro-inflammatory cytokine: Implications for drug-induced organic damage.Cell biology and toxicology · 2024Review
- HMGB1/RAGE axis in tumor development: unraveling its significance.Frontiers in oncology · 2024Review
- The multifunctional protein HMGB1: 50 years of discovery.Nature reviews. Immunology · 2023Review
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Effects of AGEs, sRAGE and HMGB1 on Clinical Outcomes in Multiple Myeloma.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023Article
- Cancer-Associated Thrombosis: Epidemiology, Pathophysiological Mechanisms, Treatment, and Risk Assessment.Clinical Medicine Insights. Oncology · 2023Review
- Thrombotic Pathogenesis and Laboratory Diagnosis in Cancer Patients, An Update.International journal of general medicine · 2023Review
- Article
- Receptor for Advanced Glycation End Products (RAGE): A Pivotal Hub in Immune Diseases.Molecules (Basel, Switzerland) · 2022Review
- The RAGE/multiligand axis: a new actor in tumor biology.Bioscience reports · 2022Review
- Role of Base Excision Repair in Innate Immune Cells and Its Relevance for Cancer Therapy.Biomedicines · 2022Review
- Review
- Macrophage scavenger receptors: Tumor support and tumor inhibition.Frontiers in oncology · 2022Review
Corrections and comments
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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 monocyte-macrophage lineage shows a high degree of diversity and plasticity. Once they infiltrate tissues, they may acquire two main functional phenotypes, being known as the classically activated type 1 macrophages (M1) and the alternative activated type 2 macrophages (M2). The M1 phenotype can be induced by bacterial products and interferon-γ and exerts a cytotoxic effect on cancer cells. Conversely, the alternatively activated M2 phenotype is induced by Il-4/IL13 and promotes tumor cell growth and vascularization. Although receptor for advanced glycation end-products (RAGE) engagement in M1 macrophages has been reported by several groups to promote inflammation, nothing is known about the functionality of RAGE in M2 macrophages. In the current study, we demonstrate that RAGE is equally expressed in both macrophage phenotypes and that RAGE activation by high-mobility group protein box1 (HMGB1) promotes protumoral activities of M2 macrophages. MKN45 cells co-cultured with M2 macrophages treated with HMGB1 at different times displayed higher invasive abilities. Additionally, conditioned medium from HMGB1-treated M2 macrophages promotes angiogenesis in vitro. RAGE-targeting knockdown abrogates these activities. Overall, the present findings suggest that HMGB1 may contribute, by a RAGE-dependent mechanism, to the protumoral activities of the M2 phenotype.
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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.