ArticleScientific reports2025
YKL-40 inhibits melanoma progression and metastasis by inducing immune cell infiltration in a mouse model.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Future Perspectives and Conclusions from Animal Models of CHI3L1-Related Inflammation-Associated Cancer.Cells · 2025Review
- Heparin-binding of the human chitinase-like protein YKL-40 is allosterically modified by chitin oligosaccharides.Biochemistry and biophysics reports · 2025Article
- FBXO31 inhibits the stemness characteristics of CD147 (+) melanoma stem cells.Open life sciences · 2025Article
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Authors and funding
14 authors.
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Abstract
YKL-40 is a glycoprotein that has been extensively studied due to its elevated expression in numerous solid tumors, and its expression is altered in melanoma, where its levels in tumor tissues are notably lower compared with those in normal skin tissues. Patients with melanoma exhibiting high YKL-40 expression have improved survival rates, suggesting a potential tumor-suppressive function of YKL-40 in melanoma. The present investigation into the ectopic expression of YKL-40 in human (A375) and murine (B16F10) melanoma cell lines demonstrated a consequential decrease in cell proliferation, migration and invasion. Furthermore, YKL-40 overexpression was associated with suppressed tumor growth in a subcutaneous melanoma mouse model and diminished tumor cell metastasis in a pulmonary metastasis model. RNA-sequencing analysis revealed that YKL-40 overexpression led to the upregulation of immune cell infiltration-related signaling pathways, including cytokine receptor interactions, natural killer cell-mediated cytotoxicity, and T and B lymphocyte receptor signaling. These findings highlight the potential of YKL-40 as a regulator of tumor-immune interactions in melanoma, highlighting its prospective utility in immunotherapy-based treatment strategies for melanoma.
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