ArticleMolecular pain
Rac1/PAK1 signaling contributes to bone cancer pain by Regulation dendritic spine remodeling in rats.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Single-cell RNA sequencing analysis of bone cancer pain model induced by Lewis lung cancer cells in male mice.Annals of medicine · 2026Article
- CSDE1 Drives Glycolysis and the Progression of Prostate Cancer Through RAC1-Dependent RAS/MAPK Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- PAK1 Is Involved in Epileptogenesis by Regulating the Synaptic Plasticity of Hippocampal Neurons Through LIMK.Neurochemical research · 2025Article
- GαInternational journal of molecular sciences · 2025Article
- Aflatoxin B1 Exposure Suppresses the Migration of Dendritic Cells by Reshaping the Cytoskeleton.International journal of molecular sciences · 2025Article
- Identifying Diagnostic Biomarkers for Electroacupuncture Treatment of Rheumatoid Arthritis Using Bioinformatic Analysis and Machine Learning Algorithms.Journal of pain research · 2025Article
- Pain - related methylation driver genes affect the prognosis of pancreatic cancer patients by altering immune function and perineural infiltration.Frontiers in genetics · 2025Article
- Systemic administration of Resolvin D1 reduces cancer-induced bone pain in mice: Lack of sex dependency in pain development and analgesia.Cancer medicine · 2024Article
- Dock4 contributes to neuropathic pain by regulating spinal synaptic plasticity in mice.Frontiers in molecular neuroscience · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone cancer pain (BCP) is severe chronic pain caused by tumor metastasis to the bones, often resulting in significant skeletal remodeling and fractures. Currently, there is no curative treatment. Therefore, insight into the underlying mechanisms could guide the development of mechanism-based therapeutic strategies for BCP. We speculated that Rac1/PAK1 signaling plays a critical role in the development of BCP. Tumor cells implantation (TCI) into the tibial cavity resulted in bone cancer-associated mechanical allodynia. Golgi staining revealed changes in the excitatory synaptic structure of WDR (Wide-dynamic range) neurons in the spinal cord, including increased postsynaptic density (PSD) length and thickness, and width of the cleft. Behavioral and western blotting test revealed that the development and persistence of pain correlated with Rac1/PAK1 signaling activation in primary sensory neurons. Intrathecal injection of NSC23766, a Rac1 inhibitor, reduced the persistence of BCP as well as reversed the remodeling of dendrites. Therefore, we concluded that activation of the Rac1/PAK1 signaling pathway in the spinal cord plays an important role in the development of BCP through remodeling of dendritic spines. Modulation of the Rac1/PAK1 pathway may be a potential strategy for BCP treatment.
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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.