ArticleTranslational oncology2026
Siglec-15 promotes a feed-forward loop between TNBC cells and macrophages via the NF-κB/DcR3/CCL18/STAT3 axis.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
M2-like tumor-associated macrophages (TAMs), recognized as a significant risk factor in tumor progression, play a crucial role in the tumor microenvironment. While Sialic acid binding Ig like Lectin 15 (Siglec-15), an well-characterized immune-checkpoint inhibitor, has been demonstrated to impact immunotherapy response and tumor progression, its role in TMAs-mediated tumor progression remains largely unclear. In this study, we demonstrated that the high expression of Siglec-15 in triple-negative breast cancer (TNBC) acts as a pivotal driver of the interaction between tumor cells and macrophages. TNBC cells with overexpressed Siglec-15 can induce the polarization of macrophages into CC chemokine ligand 18 (CCL18)
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