ArticleJournal of experimental & clinical cancer research : CR2018
Radiotherapy-induced cell death activates paracrine HMGB1-TLR2 signaling and accelerates pancreatic carcinoma metastasis.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Two weeks of hydrogen inhalation can significantly reverse adaptive and innate immune system senescence patients with advanced non-small cell lung cancer: a self-controlled study.Medical gas researchTrial
- HMGB1 promotes radiotherapy resistance in human cervical cancer HeLa cells through regulating the AMPK/mTOR signaling.World journal of surgical oncology · 2026Article
- Radiotherapy, EMP and dormancy in TME: An integrated perspective on tumor microenvironments and long-term relapse.iScience · 2026Review
- Activation of NF-κB signaling pathway in GSDME-low esophageal squamous cell carcinoma cells enhances radioresistance.Journal of translational medicine · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Toll-like receptors: versatile players in tumor.Frontiers in immunology · 2026Review
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response.Scientific reports · 2024Article
- Targeted irradiation in an autochthonous mouse model of pancreatic cancer.Disease models & mechanisms · 2024Article
- Robinin inhibits pancreatic cancer cell proliferation, EMT and inflammation via regulating TLR2-PI3k-AKT signaling pathway.Cancer cell international · 2023Article
- Toll-Like Receptors and the Response to Radiotherapy in Solid Tumors: Challenges and Opportunities.Vaccines · 2023Review
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.Frontiers in immunology · 2023Review
- HMGB1 induces radioresistance through PI3K/AKT/ATM pathway in esophageal squamous cell carcinoma.Molecular biology reports · 2022Article
- Irradiation-induced exosomal HMGB1 to confer radioresistance via the PI3K/AKT/FOXO3A signaling pathway in ESCC.Journal of translational medicine · 2022Article
- The Trinity: Interplay among Cancer Cells, Fibroblasts, and Immune Cells in Pancreatic Cancer and Implication of CD8Biomedicines · 2022Review
- HMGB1 overexpression promotes a malignant phenotype and radioresistance in ESCC.Journal of Cancer · 2022Article
- Editorial: Management of pancreatic cancer: Defining the targets for therapy.Frontiers in medicine · 2022Article
- The Role of Toll-like Receptors (TLRs) Mediated Inflammation in Pancreatic Cancer Pathophysiology.International journal of molecular sciences · 2021Review
- Identification of TLR2 Signalling Mechanisms Which Contribute to Barrett's and Oesophageal Adenocarcinoma Disease Progression.Cancers · 2021Article
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundDying cells after irradiation could promote the repopulation of surviving cancer cells leading to tumor recurrence. We aim to define the role of dying cells in promoting pancreatic cancer cells metastasis following radiotherapy.
methodsUsing the transwell system as the in vitro co-culture model, a small number of untreated pancreatic cancer cells were seeded in the upper chamber, while a larger number of lethally treated pancreatic cancer cells were seeded in the lower chamber. A series of experiments were conducted to investigate the role of dying-cell-derived HMGB1 on the invasion of pancreatic cancer in vitro and cancer metastasis in vivo. We then designed shRNA knockdown and Western blot assays to detect signaling activity.
resultsWe found that dying pancreatic cancer cells significantly promote the invasion of pancreatic cancer cells in vitro and cancer metastasis in vivo. HMGB1 gene knockdown attenuated the migration-stimulating effect of irradiated, dying cells on living pancreatic cancer cells. Finally, we showed that dying-cell-derived HMGB1 functions in a paracrine manner to affect cancer-cell migration dependent on acquiring an epithelial-mesenchymal transition (EMT) phenotype and PI3K/pAkt activation. This process is mediated by the receptor for TLR2.
conclusionOur study indicates that, during radiotherapy, dying pancreatic cancer cells activate paracrine signaling events that promote the mobility of surviving tumor cells. We suggest a strategy to inhibit HMGB1 for preventing pancreatic carcinoma relapse and metastasis.
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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.