ArticleScientific reports2017
Chemokine receptor CXCR4 regulates CaMKII/CREB pathway in spinal neurons that underlies cancer-induced bone pain.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Molecular targets in bone cancer pain: a systematic review of inflammatory cytokines.Journal of molecular medicine (Berlin, Germany) · 2024Pooled it
- CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain.Journal of neuroinflammation · 2026Article
- The function of chemokine-driven glial-neuronal interaction in chronic pain.Frontiers in neuroscience · 2026Review
- Long noncoding RNA NONRATT007487.2 drives cancer-induced bone pain progression through direct interaction with CXCL1.The Korean journal of pain · 2025Article
- Shentong Zhuyu Decoction Alleviates Neuropathic Pain in Mice by Inhibiting the NMDAR-2B Receptor-Mediated CaMKII/CREB Signaling Pathway in GABAergic Neurons of the Interpeduncular Nucleus.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Targeting TRPV6/CXCR4 complexes prevents castration-resistant prostate cancer metastasis to the bone.Signal transduction and targeted therapy · 2025Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- Lidocaine-A Promising Candidate for the Treatment of Cancer-Induced Bone Pain: A Narrative Review.Advances in therapy · 2025Review
- Mechanisms of Cancer-Induced Bone Pain.Journal of pain research · 2025Review
- The CXCL12/CXCR4 Axis: An Emerging Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
- Involvement of CXCL12/CXCR4 in CB2 receptor agonist-attenuated morphine tolerance in Walker 256 tumor-bearing rats with cancer pain.European journal of medical research · 2024Article
- Review
- CXCL12-CXCR4/CXCR7 Axis in Cancer: from Mechanisms to Clinical Applications.International journal of biological sciences · 2023Review
- Sigma-1 receptor activity in primary sensory neurons is a critical driver of neuropathic pain.Gene therapy · 2022Article
- Secondary damage and neuroinflammation in the spinal dorsal horn mediate post-thalamic hemorrhagic stroke pain hypersensitivity: SDF1-CXCR4 signaling mediation.Frontiers in molecular neuroscience · 2022Article
- Role and implications of the CXCL12/CXCR4/CXCR7 axis in atherosclerosis: still a debate.Annals of medicine · 2021Review
- Identification of key immune-related genes and immune infiltration in atrial fibrillation with valvular heart disease based on bioinformatics analysis.Journal of thoracic disease · 2021Article
- Dendritic cells in tumor microenvironment promoted the neuropathic pain via paracrine inflammatory and growth factors.Bioengineered · 2020Article
- An Investigation of the Molecular Mechanisms Underlying the Analgesic Effect of Jakyak-Gamcho Decoction: A Network Pharmacology Study.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Role of the CXCR4/ALK5/Smad3 Signaling Pathway in Cancer-Induced Bone Pain.Journal of pain research · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated that the chemokine receptor CXCR4 plays an important role in cancer-induced bone pain by activating spinal neurons and glial cells. However, the specific neuronal mechanism of CXCR4 signaling is not clear. We further report that CXCR4 contributes to the activation of the neuronal CaMKII/CREB pathway in cancer-induced bone pain. We used a tumor cell implantation (TCI) model and observed that CXCR4, p-CaMKII and p-CREB were persistently up-regulated in spinal neurons. CXCR4 also co-expressed with p-CaMKII and p-CREB, and mediated p-CaMKII and p-CREB expression after TCI. Intrathecal delivery of CXCR4 siRNA or CaMKII inhibitor AIP2 abrogated TCI-induced pain hypersensitivity and TCI-induced increase in p-CaMKII and p-CREB expression. Intrathecal injection of the principal ligand for CXCR4, SDF-1, promoted p-CaMKII and p-CREB expression in naive rats, which was prevented by post-administration of CXCR4 inhibitor Plerixafor or PLC inhibitor U73122. Plerixafor, U73122, or AIP2 also alleviated SDF-1-elicited pain behaviors. Intrathecal injection of CXCR4 siRNA significantly suppressed TCI-induced up-regulation of NMDAR1 mRNA and protein, which is a known gene target of CREB. Collectively, these results suggest that the CaMKII/CREB pathway in spinal neurons mediates CXCR4-facilitated pain hypersensitivity in cancer rats.
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