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Updated: Mar 11, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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C/EBPβ Contributes to Cancer-Induced Bone Pain by Inhibiting CD200/CD200R1 in the Spinal Cord

Dan-Yang Li1,2,3, Lin Liu1,2,3, Dai-Qiang Liu1,2,3

  • 1Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

CNS Neuroscience & Therapeutics
|March 10, 2026
PubMed
Abstract

Insights

CCAAT/enhancer binding protein β (c/EBPβ) promotes spinal microglia activation and neuroinflammation in cancer-induced bone pain (CIBP) by suppressing CD200/CD200R1 signaling. Targeting this pathway offers a potential therapeutic strategy for managing CIBP.

Area of Science:

  • Neuroscience
  • Immunology
  • Oncology

Background:

  • Cancer-induced bone pain (CIBP) is a debilitating condition in advanced cancer patients.
  • Spinal microglia activation and neuroinflammation are key pathological drivers of CIBP.
  • Current treatments for CIBP often lack efficacy.

Purpose of the Study:

  • To investigate the role of CCAAT/enhancer binding protein β (c/EBPβ) in regulating CD200R1 expression.
  • To explore the mechanism by which c/EBPβ induces microglia-mediated neuroinflammation in the spinal cord of CIBP mice.
  • To identify potential therapeutic targets for CIBP management.

Main Methods:

  • Established a CIBP mouse model via intrafemoral injection of Lewis lung cancer cells.
  • Assessed mechanical allodynia and thermal hyperalgesia using von Frey filaments and hot plate tests.
  • Utilized adeno-associated viruses to manipulate CD200R1 and c/EBPβ expression, and employed western blotting and immunofluorescence to analyze protein levels and microglia activation.

Main Results:

  • CD200/CD200R1 signaling was found to be inhibited in the spinal cords of CIBP mice.
  • Intrathecal administration of the CD200R1 agonist CD200Fc reversed pain behaviors.
  • Overexpression of CD200R1 ameliorated pain and reduced spinal neuroinflammation, while c/EBPβ was upregulated and its knockdown alleviated pain by restoring CD200R1 levels and inhibiting neuroinflammation.

Conclusions:

  • c/EBPβ suppresses the CD200/CD200R1 signaling pathway, contributing to microglial activation and neuroinflammation in CIBP.
  • This c/EBPβ-CD200/CD200R1 axis represents a potential therapeutic target for managing CIBP.
  • Targeting this pathway could offer a novel approach to alleviate bone pain in cancer patients.
Keywords:
CD200R1c/EBPβcancer‐induced bone painmicroglianeuroinflammation

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