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

CCL8, a chemokine overexpressed in ovarian cancer (OC), has drawn attention for its role in tumor progression. This study aimed to explore the function of CCL8 in OC and its effects on tumor-associated macrophages (TAMs) and related mechanisms. Bioinformatics analysis revealed a correlation between high CCL8 expression and M1 macrophage infiltration, as well as a favourable prognosis in OC patients. In vitro, CCL8 polarised THP1-derived macrophages towards an M1 phenotype, and the conditioned medium from these macrophages suppressed ES2 cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Mechanistically, CCL8-induced macrophages promoted apoptosis in OC cells via activation of the NF-κB p65 pathway, as evidenced by increased Bax and Caspase3 expression, and these effects were reversed by p65 inhibition. The findings demonstrate that CCL8 exerts a tumor-uppressive effect by inducing M1 macrophage polarisation and activating the NF-κB pathway, positioning it as a potential immunotherapeutic target in OC.