2. Academic Validation
  3. Glioblastoma cells secrete ICAM1 via FASN signaling to promote glioma-associated macrophage infiltration

Glioblastoma cells secrete ICAM1 via FASN signaling to promote glioma-associated macrophage infiltration

  • Cell Signal. 2025 Aug:132:111823. doi: 10.1016/j.cellsig.2025.111823.
Wenxin Zhang 1,  Jialin Wang 1,  Jiayu Ji 2,  Peiwen Wang 1,  Guiqiang Yuan 1,  Sheng Fang 1,  Fusheng Liu 3,  Guishan Jin 4,  Junwen Zhang 5
Affiliations

Affiliations

  • 1 Brain Tumor Research Center, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.
  • 2 Brain Tumor Research Center, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China; China Rehabilitation Science Institute, China Rehabilitation Research Center, School of Rehabilitation, Capital Medical University, Beijing, PR China.
  • 3 Brain Tumor Research Center, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China; Department of Neurosurgery, Beijing Tiantan Hosipital, Capital Medical University, Beijing, China.
  • 4 Brain Tumor Research Center, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China. Electronic address: guishanjin7@163.com.
  • 5 Brain Tumor Research Center, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China. Electronic address: jewzhang@hotmail.com.
PMID: 40252818 DOI: 10.1016/j.cellsig.2025.111823
Abstract

Glioma-associated macrophages (GAMs) constitute the most abundant subset of immune cells in the glioblastoma (GBM) microenvironment, but the underlying mechanism of intense infiltration needs to be elucidated. In this study, we found that GBM cells secrete ICAM1 via FASN signaling to promote GAM infiltration. FASN expression is correlated with GAM density in GBM patients. In vitro experiments revealed that FASN regulates the type-I interferon pathway, particularly STAT1 expression. Moreover, disrupting FASN-STAT1 signaling through the overexpression or inhibition of FASN or STAT1 in GBM cells strongly influences microglial recruitment. Additionally, ICAM1 acts as a direct transcriptional candidate of FASN-STAT1 and a paracrine soluble factor, recruiting microglia to GBM tumors. This study revealed crosstalk between GBM cells and GAMs through FASN-STAT1-ICAM1 signaling to promote microglial infiltration, suggesting potential strategies for treating GBM patients.

Keywords

FASN; Glioblastoma; ICAM1; Microglia; Recruitment; STAT1.

Figures
Products
Inhibitors & Agonists
Other Products