ArticleOncoimmunology2015
Natural Killer (NK)/melanoma cell interaction induces NK-mediated release of chemotactic High Mobility Group Box-1 (HMGB1) capable of amplifying NK cell recruitment.
Article in Oncoimmunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- HMGB1 ubiquitination inhibition and extracellular secretion, mediated by mCancer immunology, immunotherapy : CII · 2026Article
- Human NK cells and cancer.Oncoimmunology · 2024Review
- Immunomodulatory effects of immune cell-derived extracellular vesicles in melanoma.Frontiers in immunology · 2024Review
- CXCL12/CXCR4 Axis is Involved in the Recruitment of NK Cells by HMGB1 Contributing to Persistent Airway Inflammation and AHR During the Late Stage of RSV Infection.Journal of microbiology (Seoul, Korea) · 2023Article
- Murine models to study human NK cells in human solid tumors.Frontiers in immunology · 2023Review
- Anticancer traits of chimeric antigen receptors (CARs)-Natural Killer (NK) cells as novel approaches for melanoma treatment.BMC cancer · 2022Article
- Paralysis of the cytotoxic granule machinery is a new cancer immune evasion mechanism mediated by chitinase 3-like-1.Journal for immunotherapy of cancer · 2021Article
- Functional Amino Acids and Autophagy: Diverse Signal Transduction and Application.International journal of molecular sciences · 2021Review
- miR-142-3p reduces the viability of human cervical cancer cells by negatively regulating the cytoplasmic localization of HMGB1.Experimental and therapeutic medicine · 2021Article
- Article
- Role of HMGB1 in Chemotherapy-Induced Peripheral Neuropathy.International journal of molecular sciences · 2020Review
- Role of the Main Non HLA-Specific Activating NK Receptors in Pancreatic, Colorectal and Gastric Tumors Surveillance.Cancers · 2020Review
- U3-1402 sensitizes HER3-expressing tumors to PD-1 blockade by immune activation.The Journal of clinical investigation · 2020Article
- miRNAs in NK Cell-Based Immune Responses and Cancer Immunotherapy.Frontiers in cell and developmental biology · 2020Review
- NK Cell-Based Immunotherapy for Hematological Malignancies.Journal of clinical medicine · 2019Review
- The Uncovered Role of Immune Cells and NK Cells in the Regulation of Bone Metastasis.Frontiers in endocrinology · 2019Review
- Mechanism and medical implications of mammalian autophagy.Nature reviews. Molecular cell biology · 2018Review
- Redox control of cancer cell destruction.Redox biology · 2018Review
- Hypoxia Modifies the Transcriptome of Human NK Cells, Modulates Their Immunoregulatory Profile, and Influences NK Cell Subset Migration.Frontiers in immunology · 2018Article
- Profile of differentially expressed Toll-like receptor signaling genes in the natural killer cells of patients with Sézary syndrome.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we characterize a new mechanism by which Natural Killer (NK) cells may amplify their recruitment to tumors. We show that NK cells, upon interaction with melanoma cells, can release a chemotactic form of High Mobility Group Box-1 (HMGB1) protein capable of attracting additional activated NK cells. We first demonstrate that the engagement of different activating NK cell receptors, including those mainly involved in tumor cell recognition can induce the active release of HMGB1. Then we show that during NK-mediated tumor cell killing two HMGB1 forms are released, each displaying a specific electrophoretic mobility possibly corresponding to a different redox status. By the comparison of normal and perforin-defective NK cells (which are unable to kill target cells) we demonstrate that, in NK/melanoma cell co-cultures, NK cells specifically release an HMGB1 form that acts as chemoattractant, while dying tumor cells passively release a non-chemotactic HMGB1. Finally, we show that Receptor for Advanced Glycation End products is expressed by NK cells and mediates HMGB1-induced NK cell chemotaxis. Proteomic analysis of NK cells exposed to recombinant HMGB1 revealed that this molecule, besides inducing immediate chemotaxis, also promotes changes in the expression of proteins involved in the regulation of the cytoskeletal network. Importantly, these modifications could be associated with an increased motility of NK cells. Thus, our findings allow the definition of a previously unidentified mechanism used by NK cells to amplify their response to tumors, and provide additional clues for the emerging role of HMGB1 in immunomodulation and tumor immunity.
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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.