ArticleJournal of neuro-oncology2008
HMGB1 as an autocrine stimulus in human T98G glioblastoma cells: role in cell growth and migration.
Article in Journal of neuro-oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- RAGE signaling inhibition prevents the malignant phenotypes of pancreatic ductal adenocarcinoma cells.Scientific reports · 2026Article
- HMGB1/RAGE axis in tumor development: unraveling its significance.Frontiers in oncology · 2024Review
- Flavonoids Regulate Redox-Responsive Transcription Factors in Glioblastoma and Microglia.Cells · 2023Article
- The Importance of M1-and M2-Polarized Macrophages in Glioma and as Potential Treatment Targets.Brain sciences · 2023Review
- Inhibition of DAMP actions in the tumoral microenvironment using lactoferrin-glycyrrhizin conjugate for glioblastoma therapy.Biomaterials research · 2023Article
- Hypoxia-induced HMGB1 promotes glioma stem cells self-renewal and tumorigenicity via RAGE.iScience · 2022Article
- Necrotic reshaping of the glioma microenvironment drives disease progression.Acta neuropathologica · 2022Review
- Novel understanding of high mobility group box-1 in the immunopathogenesis of incisional hernias.Expert review of clinical immunology · 2019Review
- Upregulated necroptosis-pathway-associated genes are unfavorable prognostic markers in low-grade glioma and glioblastoma multiforme.Translational cancer research · 2019Article
- Suppression of HMGB1 Released in the Glioblastoma Tumor Microenvironment Reduces Tumoral Edema.Molecular therapy oncolytics · 2019Article
- Anticancer effects of a non-narcotic opium alkaloid medicine, papaverine, in human glioblastoma cells.PloS one · 2019Article
- HMGB1-Induced p62 Overexpression Promotes Snail-Mediated Epithelial-Mesenchymal Transition in Glioblastoma Cells via the Degradation of GSK-3β.Theranostics · 2019Article
- Article
- MicroRNA-142-3p inhibits proliferation and induces apoptosis by targeting the high-mobility group box 1 via the Wnt/β-catenin signaling pathway in glioma.International journal of clinical and experimental pathology · 2018Article
- Alarmins and immunity.Immunological reviews · 2017Review
- Paradoxical Role of High Mobility Group Box 1 in Glioma: A Suppressor or a Promoter?Oncology reviews · 2017Review
- Pivotal role of high-mobility group box 1 (HMGB1) signaling pathways in glioma development and progression.Journal of molecular medicine (Berlin, Germany) · 2016Review
- The brain tissue response to surgical injury and its possible contribution to glioma recurrence.Journal of neuro-oncology · 2016Review
- MicroRNA-218 modulates activities of glioma cells by targeting HMGB1.American journal of translational research · 2016Article
- Expression of the receptor for advanced glycation end products, a target for high mobility group box 1 protein, and its role in chronic recalcitrant rhinosinusitis with nasal polyps.Archivum immunologiae et therapiae experimentalis · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HMGB1 (high mobility group box 1 protein) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, mainly through RAGE (the receptor for advanced glycation end products); HMGB1-RAGE interactions have been found to be important in a number of cancers. We investigated whether HMGB1 is an autocrine factor in human glioma cells. Western blots showed HMGB1 and RAGE expression in human malignant glioma cell lines. HMGB1 induced a dose-dependent increase in cell proliferation, which was found to be RAGE-mediated and involved the MAPK/ERK pathway. Moreover, in a wounding model, it induced a significant increase in cell migration, and RAGE-dependent activation of Rac1 was crucial in giving the tumour cells a motile phenotype. The fact that blocking DNA replication with anti-mitotic agents did not reduce the distance migrated suggests the independence of the proliferative and migratory effects. We also found that glioma cells contain HMGB1 predominantly in the nucleus, and cannot secrete it constitutively or upon stimulation; however, necrotic glioma cells can release HMGB1 after it has translocated from the nucleus to cytosol. These findings provide the first evidence supporting the existence of HMGB1/RAGE signalling pathways in human glioblastoma cells, and suggest that HMGB1 may play an important role in the relationship between necrosis and malignancy in glioma tumours by acting as an autocrine factor that is capable of promoting the growth and migration of tumour cells.
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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.