ArticleJournal of neuroinflammation2014
NFκB-mediated CXCL1 production in spinal cord astrocytes contributes to the maintenance of bone cancer pain in mice.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026Review
- Therapeutic applications of mesenchymal stem cell-derived extracellular vesicles in pain management: A narrative review of emerging evidence and future directions.World journal of stem cells · 2026Review
- Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.Neuroscience bulletin · 2025Review
- Article
- Long noncoding RNA NONRATT007487.2 drives cancer-induced bone pain progression through direct interaction with CXCL1.The Korean journal of pain · 2025Article
- Facilitated α-synuclein oligomer sharing among glial cells by a centrally acting connexin inhibitor attenuates a rapidly progressive multiple system atrophy-cerebellar type model by reducing the neuronal α-synuclein burden.Acta neuropathologica communications · 2025Article
- Adipocyte-derived IL6 and triple-negative breast cancer cell-derived CXCL1 co-activate STAT3/NF-κB pathway to mediate the crosstalk between adipocytes and triple-negative breast cancer cells.Cell death discovery · 2025Article
- Cancer pain: molecular mechanisms and management.Molecular biomedicine · 2025Review
- Daphnetin alleviates neuropathic pain in chronic constrictive injury ratsPharmaceutical biology · 2023Article
- Evaluation of pain related behaviors and disease related outcomes in an immunocompetent mouse model of prostate cancer induced bone pain.Journal of bone oncology · 2023Article
- A key protein fromIBRO neuroscience reports · 2023Article
- Perturbations in Neuroinflammatory Pathways Are Associated With a Worst Pain Profile in Oncology Patients Receiving Chemotherapy.The journal of pain · 2023Article
- Revolutionizing orofacial pain management: the promising potential of stem cell therapy.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Growth Regulated Oncogene-α Upregulates TNF-α and COX-2 and Activates NOD1/RIPK2 mediated-MAPK Pathway in Head and Neck Squamous Cell Carcinoma.Journal of Cancer · 2023Article
- Collaborative Action of Microglia and Astrocytes Mediates Neutrophil Recruitment to the CNS to Defend againstInternational journal of molecular sciences · 2022Article
- The Genesis of Pain in Osteoarthritis: Inflammation as a Mediator of Osteoarthritis Pain.Clinics in geriatric medicine · 2022Review
- CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats.Molecular pain · 2022Article
- CXCR2 Receptor: Regulation of Expression, Signal Transduction, and Involvement in Cancer.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBone cancer pain (BCP) is one of the most disabling factors in patients suffering from primary bone cancer or bone metastases. Recent studies show several chemokines (for example, CCL2, CXCL10) in the spinal cord are involved in the pathogenesis of BCP. Here we investigated whether and how spinal CXCL1 contributes to BCP.
methodsMouse prostate tumor cell line, RM-1 cells were intramedullary injected into the femur to induce BCP. The mRNA expression of CXCL1 and CXCR2 was detected by quantitative real-time PCR. The protein expression and distribution of CXCL1, NFκB, and CXCR2 was examined by immunofluorescence staining and western blot. The effect of CXCL1 neutralizing antibody, NFκB antagonist, and CXCR2 antagonist on pain hypersensitivity was checked by behavioral testing.
resultsIntramedullary injection of RM-1 cells into the femur induced cortical bone damage and persistent (>21 days) mechanical allodynia and heat hyperalgesia. Tumor cell inoculation also produced CXCL1 upregulation in activated astrocytes in the spinal cord for more than 21 days. Inhibition of CXCL1 by intrathecal administration of CXCL1 neutralizing antibody at 7 days after inoculation attenuated mechanical allodynia and heat hyperalgesia. In cultured astrocytes, TNF-α induced robust CXCL1 expression, which was dose-dependently decreased by NFκB inhibitor. Furthermore, inoculation induced persistent NFκB phosphorylation in spinal astrocytes. Intrathecal injection of NFκB inhibitor attenuated BCP and reduced CXCL1 increase in the spinal cord. Finally, CXCR2, the primary receptor of CXCL1, was upregulated in dorsal horn neurons after inoculation. Inhibition of CXCR2 by its selective antagonist SB225002 attenuated BCP.
conclusionNFκB mediates CXCL1 upregulation in spinal astrocytes in the BCP model. In addition, CXCL1 may be released from astrocytes and act on CXCR2 on neurons in the spinal cord and be involved in the maintenance of BCP. Inhibition of the CXCL1 signaling may provide a new therapy for BCP management.
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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.