ReviewJournal of molecular medicine (Berlin, Germany)2016
Pivotal role of high-mobility group box 1 (HMGB1) signaling pathways in glioma development and progression.
Review in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 69 citations in OpenAlex.
- HMGB1 as Double-Edged Regulator of Cancer Therapy: Mechanistic Roles in Chemotherapy Resistance and Immunotherapy Response.OncoTargets and therapy · 2026Review
- Radiodynamic Therapy for High-Grade Glioma in Normoxic and Hypoxic Environments for High-Grade Glioma.Cancers · 2025Article
- Innate Immune Signaling in Gliomas: Regulatory Mechanisms and Targeting Potential in Tumor Progression.Life (Basel, Switzerland) · 2025Review
- Viral expression of NE/PPE enhances anti-colorectal cancer efficacy of oncolytic adenovirus by promoting TAM M1 polarization to reverse insufficient effector memory/effector CD8Journal of experimental & clinical cancer research : CR · 2025Article
- Ferroptosis in glioma therapy: advancements in sensitizing strategies and the complex tumor-promoting roles.Brain research · 2024Review
- HMGB1/RAGE axis in tumor development: unraveling its significance.Frontiers in oncology · 2024Review
- Contributing Role of High Mobility Group Box 1 Signaling in Oral Cancer Development and Therapy.Life (Basel, Switzerland) · 2023Review
- Inhibition of DAMP actions in the tumoral microenvironment using lactoferrin-glycyrrhizin conjugate for glioblastoma therapy.Biomaterials research · 2023Article
- RAGE ablation attenuates glioma progression and enhances tumor immune responses by suppressing galectin-3 expression.Neuro-oncology · 2023Article
- circ_0008285 Regulates Glioma Progression via the miR-384/HMGB1 Axis.International journal of genomics · 2023Article
- Autophagy-based unconventional secretion of HMGB1 in glioblastoma promotes chemosensitivity to temozolomide through macrophage M1-like polarization.Journal of experimental & clinical cancer research : CR · 2022Article
- A novel therapeutic strategy of multimodal nanoconjugates for state-of-the-art brain tumor phototherapy.Journal of nanobiotechnology · 2022Article
- Up-regulation of LINC00665 contributes to the progression of glioma and correlates with its MRI characteristics.American journal of translational research · 2022Article
- Irradiation-induced polyploid giant cancer cells are involved in tumor cell repopulation via neosis.Molecular oncology · 2021Article
- miR-665 is downregulated in glioma and inhibits tumor cell proliferation, migration and invasion by targeting high mobility group box 1.Oncology letters · 2021Article
- Temozolomide Treatment Induces HMGB1 to Promote the Formation of Glioma Stem Cells via the TLR2/NEAT1/Wnt Pathway in Glioblastoma.Frontiers in cell and developmental biology · 2021Article
- HMGB1 regulates SNAI1 during NSCLC metastasis, both directly, through transcriptional activation, and indirectly, in a RSF1-IT2-dependent manner.Molecular oncology · 2020Article
- Local and Systemic Immune Dysregulation Alters Glioma Growth in Hyperglycemic Mice.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Neutrophil extracellular traps mediate the crosstalk between glioma progression and the tumor microenvironmentCancer biology & medicine · 2020Observational
- LINC00662 sponges miR-107 accelerating the invasiveness and proliferation of glioma cells.Journal of Cancer · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human gliomas represent the most common type of intracranial tumors, with highest morbidity and mortality. They are characterized by excessive invasiveness and cell proliferation while their unclear boundaries predispose to tumor recurrence soon after conventional treatment. Elucidation of the molecular mechanisms implicated in their development and/or treatment resistance is highly demanded. The high-mobility group box 1 (HMGB1) protein, a highly conserved nuclear protein that functions as a chromatin-binding factor, facilitating nucleosome stabilization and regulating gene transcription, has been implicated in glioma formation and progression. Extracellular released HMGB1 binds to high-affinity receptors, including the receptor for advanced glycation end-products (RAGE) and toll-like receptor (TLR)-2, TLR-4, and TLR-9. Upon receptor binding, HMGB1 triggers the activation of key signaling pathways and immune responses, involved in the regulation of cell growth, differentiation, motility, and apoptosis. Based on the type of receptor and/or cell, HMGB1 is capable to promote oncogenesis or suppress tumor growth, thus affecting treatment efficacy. Herein, we discuss recent evidence implicating HMGB1 in glioma cell differentiation, proliferation, and metastasis with both clinical and prognostic significance. In addition, potential therapeutic approaches to target this protein in order to reduce chemoresistance of glioma cells are also addressed.
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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.