ArticleCell death & disease2025
Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer.
Article in Cell death & disease, 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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Who cites it
3 citing papers in PubMed.
- Tumor-Induced Splenic Remodeling: Mechanisms of Systemic Immunosuppression and Emerging Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Myeloid-derived suppressor cells in colorectal cancer: mechanisms of immunosuppression, therapy resistance and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Multicellular immunosuppressive networks in microsatellite-stable colorectal cancer: CD8+ T cell exclusion, dysfunction, exhaustion, and therapeutic implications.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Myeloid-derived suppressor cells (MDSC) are a heterogeneous group of immunosuppressive cells that expand in tumors due to impaired differentiation into macrophages (MΦ), dendritic cells (DC), or granulocytes. Despite extensive research, the mechanisms governing their differentiation remain incompletely understood. Transforming growth factor β1 (Tgfβ1), abundant in the tumor microenvironment (TME), regulates cellular differentiation via the classical Smad2/3 pathway, yet paradoxically fails to drive MDSC maturation. In this study, we demonstrate that Smad3 is significantly downregulated in MDSC from colorectal cancer (CRC) patients and tumor-bearing mouse models, impairing monocytic lineage maturation. Myeloid-specific Smad3 overexpression promotes the differentiation of MO-MDSC into mature MΦ and DC, enhances MHC-II expression, and reduces immunosuppressive molecules, thereby attenuating tumor progression. Mechanistically, Tgfβ1 induces MO-MDSC expansion via the non-classical PI3K/AKT pathway, which is counteracted by Smad3 overexpression. Furthermore, Mettl3-mediated m
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