ArticleOncology reports2020
High mobility group box 1 induces bone pain associated with bone invasion in a mouse model of advanced head and neck cancer.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 16 citations in OpenAlex.
- Role of TRP Channels in Cancer-Induced Bone Pain.International journal of molecular sciences · 2025Review
- Peripheral Mechanism of Cancer-Induced Bone Pain.Neuroscience bulletin · 2024Review
- The mechanism of high mobility group box-1 protein and its bidirectional regulation in tumors.Biomolecules & biomedicine · 2024Review
- Contributing Role of High Mobility Group Box 1 Signaling in Oral Cancer Development and Therapy.Life (Basel, Switzerland) · 2023Review
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Electroacupuncture Improves Blood-Brain Barrier and Hippocampal Neuroinflammation in SAMP8 Mice by Inhibiting HMGB1/TLR4 and RAGE/NADPH Signaling Pathways.Chinese journal of integrative medicine · 2023Article
- Mouse Models of Tumor Bone Metastasis and Invasion for Studying CCN Proteins.Methods in molecular biology (Clifton, N.J.) · 2023Article
- circ‑LRP6 contributes to osteosarcoma progression by regulating the miR‑141‑3p/HDAC4/HMGB1 axis.International journal of oncology · 2022Article
- TRPV1 in dorsal root ganglion contributed to bone cancer pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced head and neck cancer (HNC) can invade facial bone and cause bone pain, thus posing a significant challenge to the quality of life of patients presenting with advanced HNC. The present study was designed to investigate HNC bone pain (HNC‑BP) in an intratibial mouse xenograft model that utilized an HNC cell line (SAS cells). These mice develop HNC‑BP that is associated with an expression of phosphorylated ERK1/2 (pERK1/2), which is a molecular indicator of neuron excitation in dorsal root ganglia (DRG) sensory neurons. Our experiments demonstrated that the inhibition of high mobility group box 1 (HMGB1) by short hairpin (shRNA) transduction, HMGB1 neutralizing antibody, and HMGB1 receptor antagonist suppressed the HNC‑BP and the pERK1/2 expression in DRG. It was also observed that HNC‑derived HMGB1 increased the expression of the acid‑sensing nociceptor, transient receptor potential vanilloid 1 (TRPV1), which is a major cause of osteoclastic HNC‑BP in DRG. Collectively, our results demonstrated that HMGB1 originating in HNC evokes HNC‑BP via direct HMGB1 signaling and hypersensitization for the acid environment in sensory neurons.
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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.