ArticleCancer immunology research2015
SOCS3 Deficiency in Myeloid Cells Promotes Tumor Development: Involvement of STAT3 Activation and Myeloid-Derived Suppressor Cells.
Article in Cancer immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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
40 citing papers in PubMed, 55 citations in OpenAlex.
- Differential peripheral immune dynamics underlie therapeutic response to chemotherapy and chemoimmunotherapy in triple-negative breast cancer.ImmunoHorizons · 2026Article
- The suppressor of cytokine signaling 3 regulates glioma stem cell maintenance and immune microenvironment through signal transducer and activator of transcription 3 signaling.Journal of cell communication and signaling · 2026Article
- Identification and functional validation of lipid droplet-associated prognostic biomarkers in breast cancer via integrative multi-omics and machine learning approaches.International journal of clinical oncology · 2026Article
- Review
- New insight into the role of SOCS family in immune regulation and autoimmune pathogenesis.Journal of advanced research · 2026Review
- SOCS3: An Immunological Biomarker Offering Potential Therapeutic Targets for Malignant Tumors.Biological procedures online · 2025Review
- Dihydrotestosterone-androgen receptor signaling suppresses EBV-positive gastric cancer through DNA demethylation-mediated viral reactivation.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2025Article
- Natural saponins and macrophage polarization: Mechanistic insights and therapeutic perspectives in disease management.Frontiers in pharmacology · 2025Review
- Understanding the immunosuppressive microenvironment of glioma: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
- Selective activation of STAT3 and STAT5 dictates the fate of myeloid progenitor cells.Cell death discovery · 2023Article
- PTK6 inhibits autophagy to promote uveal melanoma tumorigenesis by binding to SOCS3 and regulating mTOR phosphorylation.Cell death & disease · 2023Article
- Socs3b regulates the development and function of innate immune cells in zebrafish.Frontiers in immunology · 2023Article
- Interaction Between microRNAs and Myeloid-Derived Suppressor Cells in Tumor Microenvironment.Frontiers in immunology · 2022Review
- Myeloid-derived suppressor cell: A crucial player in autoimmune diseases.Frontiers in immunology · 2022Review
- miR-aculous new avenues for cancer immunotherapy.Frontiers in immunology · 2022Review
- Polymorphonuclear Myeloid-Derived Cells That Contribute to the Immune Paralysis Are Generated in the Early Phase of Sepsis via PD-1/PD-L1 Pathway.Infection and immunity · 2021Article
- Developmental pathways of myeloid-derived suppressor cells in neoplasia.Cellular immunology · 2021Review
- Review
- SOCS Proteins in Immunity, Inflammatory Diseases, and Immune-Related Cancer.Frontiers in medicine · 2021Review
- Novel Characterization of Myeloid-Derived Suppressor Cells in Tumor Microenvironment.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Suppressor of cytokine signaling (SOCS) proteins are negative regulators of the JAK/STAT pathway and generally function as tumor suppressors. The absence of SOCS3 in particular leads to heightened activation of the STAT3 transcription factor, which has a striking ability to promote tumor survival while suppressing antitumor immunity. We report for the first time that genetic deletion of SOCS3, specifically in myeloid cells, significantly enhances tumor growth, which correlates with elevated levels of myeloid-derived suppressor cells (MDSC) in the tumor microenvironment, and diminishes CD8(+) T-cell infiltration in tumors. The importance of MDSCs in promoting tumor growth is documented by reduced tumor growth upon depletion of MDSCs. Furthermore, SOCS3-deficient bone-marrow-derived cells exhibit heightened STAT3 activation and preferentially differentiate into the Gr-1(+)CD11b(+)Ly6G(+) MDSC phenotype. Importantly, we identify G-CSF as a critical factor secreted by the tumor microenvironment that promotes development of MDSCs via a STAT3-dependent pathway. Abrogation of tumor-derived G-CSF reduces the proliferation and accumulation of Gr-1(+)CD11b(+) MDSCs and inhibits tumor growth. These findings highlight the critical function of SOCS3 as a negative regulator of MDSC development and function via inhibition of STAT3 activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.