ArticleJournal of translational medicine2025
Tumor cell-derived osteopontin promotes tumor fibrosis indirectly via tumor-associated macrophages.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- Spatial multi omic profiling maps hypoxia-driven pro-fibrotic SPP1Experimental hematology & oncology · 2026Article
- Review
- SPP1+ Macrophages and the Orchestration of Spatially Organized Immunosuppression in Cancer.Biomedicines · 2026Review
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Orchestrating the pre-metastatic niche: roles of stromal mediators and immune cells in metastatic progression and therapeutic targeting.Frontiers in immunology · 2026Review
- Review
- The Dual Nature of Cellular Senescence: From Aging Signature to Regenerative Catalyst.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundHigh fibrosis of the tumor microenvironment (TME) not only impedes the effective infiltration of T cells but also serves as a physical barrier to inhibit the penetration of chemotherapy drugs. Triple-negative breast cancer (TNBC) is characterized by significant infiltration of tumor-associated macrophages (TAMs) and high fibrosis. However, the mechanism of high fibrosis in such tumors is still under debate.
methodsWe first investigated the correlation between tumor-derived osteopontin (OPN) and tumor fibrosis as well as TAM enrichment using a tumor model characterized by OPN genetic inactivation or overexpression. We further compared the effects of macrophage depletion on tumor fibrosis in mice bearing TNBC tumors (4T1
resultsOur study revealed that OPN secretion by tumor cells correlates positively with both tumor fibrosis and TAM enrichment. Specifically, within the enriched TAM population, Ly6C
conclusionsThis study shows that tumor-derived OPN primarily drives TAM enrichment in mouse cancer model, indirectly promoting tumor fibrosis through Ly6C
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