ArticleCell research2017
Intracellular HMGB1 as a novel tumor suppressor of pancreatic cancer.
Article in Cell research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.
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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
86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 135 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Value of HMGB1 expression for assessing gastric cancer severity: a systematic meta-analysis.The Journal of international medical research · 2021Pooled it
- Caspase-1/11 deficiency and cold exposure enhance the anti-tumor activity of brown adipose tissue secretome against breast cancer cells.Cancer & metabolism · 2026Article
- The Multi-Target lncRNA-miRNA-mRNA TRIAD in Pancreatic Cancer Diagnosis and Therapy.International journal of molecular sciences · 2026Review
- Thrombomodulin Mitigates the Progression of Hepatocellular Carcinoma in Steatotic Liver.Journal of hepatocellular carcinoma · 2026Article
- HMGB1 as Double-Edged Regulator of Cancer Therapy: Mechanistic Roles in Chemotherapy Resistance and Immunotherapy Response.OncoTargets and therapy · 2026Review
- GULP1 Fuels Resistance to PD-1 Blockade through Lipid-Mediated Metabolic Reprogramming of Tumor-Associated Macrophages in Gastric Cancer.Cancer communications (London, England) · 2026Article
- Autophagy: a novel target in order to overcome drug resistance in pancreatic adenocarcinoma.Open biology · 2025Review
- Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- HMGB1 Deficiency Occurs in a Broad Range of Human Cancers and Is Often Associated with Unfavorable Tumor Phenotype.Diagnostics (Basel, Switzerland) · 2025Article
- Article
- CYP51A1 drives resistance to pH-dependent cell death in pancreatic cancer.Nature communications · 2025Article
- HMGB1: new biomarker and therapeutic target of autoimmune and autoinflammatory skin diseases.Frontiers in immunology · 2025Review
- Extracellular NCOA4 is a mediator of septic death by activating the AGER-NFKB pathway.Autophagy · 2024Article
- NFE2L2 and SLC25A39 drive cuproptosis resistance through GSH metabolism.Scientific reports · 2024Article
- Macroautophagy/autophagy promotes resistance to KRASCancer letters · 2024Article
- Icaritin Exerts Anti-Cancer Effects through Modulating Pyroptosis and Immune Activities in Hepatocellular Carcinoma.Biomedicines · 2024Article
- RBBP4: A novel diagnostic and prognostic biomarker for non-small-cell lung cancer correlated with autophagic cell death.Cancer medicine · 2024Article
- LncRNAs as nodes for the cross-talk between autophagy and Wnt signaling in pancreatic cancer drug resistance.International journal of biological sciences · 2024Review
- TXNDC12 inhibits lipid peroxidation and ferroptosis.iScience · 2023Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) driven by oncogenic K-Ras remains among the most lethal human cancers despite recent advances in modern medicine. The pathogenesis of PDAC is partly attributable to intrinsic chromosome instability and extrinsic inflammation activation. However, the molecular link between these two events in pancreatic tumorigenesis has not yet been fully established. Here, we show that intracellular high mobility group box 1 (HMGB1) remarkably suppresses oncogenic K-Ras-driven pancreatic tumorigenesis by inhibiting chromosome instability-mediated pro-inflammatory nucleosome release. Conditional genetic ablation of either single or both alleles of HMGB1 in the pancreas renders mice extremely sensitive to oncogenic K-Ras-driven initiation of precursor lesions at birth, including pancreatic intraepithelial neoplasms, intraductal papillary mucinous neoplasms, and mucinous cystic neoplasms. Loss of HMGB1 in the pancreas is associated with oxidative DNA damage and chromosomal instability characterized by chromosome rearrangements and telomere abnormalities. These lead to inflammatory nucleosome release and propagate K-Ras-driven pancreatic tumorigenesis. Extracellular nucleosomes promote interleukin 6 (IL-6) secretion by infiltrating macrophages/neutrophils and enhance oncogenic K-Ras signaling activation in pancreatic lesions. Neutralizing antibodies to IL-6 or histone H3 or knockout of the receptor for advanced glycation end products all limit K-Ras signaling activation, prevent cancer development and metastasis/invasion, and prolong animal survival in Pdx1-Cre;K-Ras
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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.