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CCL8 suppresses ovarian cancer progression via M1 macrophage polarization and NF-κB-mediated apoptosis

Jie Fang1, Xinyue Zhao2, Jin Wang2

  • 1Department of Gynecology, The Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, 212001, Jiangsu, China. fangjie070@163.com.

Scientific Reports
|December 17, 2025
PubMed

Insights

Chemokine CCL8, elevated in ovarian cancer (OC), suppresses tumor growth by activating M1 macrophages and the NF-κB pathway. This suggests CCL8 as a potential immunotherapy target for OC.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Chemokine CCL8 is overexpressed in ovarian cancer (OC) and implicated in tumor progression.
  • Tumor-associated macrophages (TAMs) play a complex role in cancer, with M1 polarization often associated with anti-tumor immunity.

Purpose of the Study:

  • To investigate the function of CCL8 in ovarian cancer.
  • To determine CCL8's effects on tumor-associated macrophages (TAMs) and elucidate underlying mechanisms.

Main Methods:

  • Bioinformatics analysis of patient data.
  • In vitro cell culture experiments using THP1-derived macrophages and ES2 ovarian cancer cells.
  • Assessment of macrophage polarization, cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and apoptosis.
  • Analysis of the NF-κB p65 signaling pathway.

Main Results:

  • High CCL8 expression correlated with M1 macrophage infiltration and better prognosis in OC patients.
  • CCL8 induced M1 polarization in macrophages.
  • Conditioned medium from CCL8-polarized macrophages inhibited OC cell proliferation, migration, invasion, and EMT.
  • CCL8-induced macrophages promoted OC cell apoptosis via NF-κB p65 pathway activation (increased Bax and Caspase3).
  • p65 inhibition reversed these anti-tumor effects.

Conclusions:

  • CCL8 exhibits tumor-suppressive functions in ovarian cancer.
  • CCL8 exerts its effects by promoting M1 macrophage polarization and activating the NF-κB pathway.
  • CCL8 represents a potential immunotherapeutic target for ovarian cancer.
Keywords:
CCL8MacrophagesNF-κBOvarian cancerP65

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