ArticleJournal of veterinary science2025
Protumor effect of CXCL10/CXCR3 axis in canine mammary gland tumor.
Article in Journal of veterinary science, 2025. 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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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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Authors and funding
8 authors.
Funding
Abstract
importanceChemokines and their receptors play integral roles in carcinogenesis. CXC motif chemokine receptor 3 (CXCR3) in T cells mediates anti-tumor effects, whereas CXCR3 in malignant cells promotes proliferation and metastasis. Although the role of CXCR3 has been well-documented in human cancers, including breast cancer, its function in canine tumors remains largely unexplored.
objectiveThis study aimed to investigate the effects of CXCR3 and its ligand interaction in canine mammary gland tumor (cMGT) cells.
methodsCXCR3 expression in two cMGT cell lines, CIPp and CIPm, was evaluated using real-time quantitative polymerase chain reaction, western blotting, and flow cytometry. CXC motif chemokine ligand 10 (CXCL10)-induced changes in CXCR3 protein expression in cMGT cells were assessed using membrane fractionation assays. Cell proliferation and migration in response to CXCL10 treatment were analyzed using Cell Counting Kit-8 and wound-healing assays, respectively. Additionally, the downstream molecular mechanisms of the CXCL10/CXCR3 axis were examined.
resultsCXCR3 expression was significantly higher in CIPm than in CIPp cells. In both the cMGT cell lines, CXCL10 treatment reduced CXCR3 expression on the cell membrane in a dose- and time-dependent manner. The CXCR10/CXCR3 axis promoted cell proliferation and migration in cMGT cells. CXCL10/CXCR3 interaction upregulated the phosphorylation of AKT1 and ERK. CONCLUSIONS AND RELEVANCE: This study demonstrates that the CXCL10/CXCR3 axis may contribute to the pathogenesis of cMGTs by promoting tumor cell proliferation and migration. CXCR3 signaling represents a potential therapeutic target for cMGTs.
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