ArticleCancer immunology research2023
Syntaphilin Regulates Neutrophil Migration in Cancer.
Article in Cancer immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The trial behind it
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Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- IL-37/IL-1R8 axis: a novel major mechanism of control at the interface between tumor and immune cells.Oncoimmunology · 2026Review
- Syntaphilin Regulates Epithelial-Mesenchymal Transition and Metastasis in Gastric Cancer via the FAK/NF-κB/MMP-9 Signaling Pathway.International journal of molecular sciences · 2026Article
- Article
- Harnessing myeloid cell plasticity for cancer therapy.Nature cancer · 2026Review
- HIF-1α suppresses SNPH expression to facilitate liver metastasis of colorectal cancer through regulating mitochondrial dynamics and filopodia formation.Cell death & disease · 2026Article
- Decoding mitochondrial signaling: neutrophil-tumor cell crosstalk in orchestrating cancer progression.Journal of translational medicine · 2026Review
- Orchestrating the pre-metastatic niche: roles of stromal mediators and immune cells in metastatic progression and therapeutic targeting.Frontiers in immunology · 2026Review
- Syntaphilin loss enhances mitochondrial axonal transport and neuromuscular junction formation in a human stem cell derived neuromuscular assembloid model.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025Review
- Neutrophils in cancer: At the crucial crossroads of anti-tumor and pro-tumor.Cancer communications (London, England) · 2025Review
- Tumor-associated neutrophils and neutrophil extracellular traps in lung cancer: antitumor/protumor insights and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Research status of regenerative difficulties after central nervous system injury.Regenerative therapy · 2025Review
- Triple-negative breast cancer modifies the systemic immune landscape and alters neutrophil functionality.NPJ breast cancer · 2025Article
- [Research Progress of Tumor-associated Neutrophils in the Occurrence and Development of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Metabolic reprogramming of tumor-associated neutrophils in tumor treatment and therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
Pathologically activated neutrophils (PMN) with immunosuppressive activity, which are termed myeloid-derived suppressor cells (PMN-MDSC), play a critical role in regulating tumor progression. These cells have been implicated in promoting tumor metastases by contributing to premetastatic niche formation. This effect was facilitated by enhanced spontaneous migration of PMN from bone marrow to the premetastatic niches during the early-stage of cancer development. The molecular mechanisms underpinning this phenomenon remained unclear. In this study, we found that syntaphilin (SNPH), a cytoskeletal protein previously known for anchoring mitochondria to the microtubule in neurons and tumor cells, could regulate migration of PMN. Expression of SNPH was decreased in PMN from tumor-bearing mice and patients with cancer as compared with PMN from tumor-free mice and healthy donors, respectively. In Snph-knockout (SNPH-KO) mice, spontaneous migration of PMN was increased and the mice showed increased metastasis. Mechanistically, in SNPH-KO mice, the speed and distance travelled by mitochondria in PMN was increased, rates of oxidative phosphorylation and glycolysis were elevated, and generation of adenosine was increased. Thus, our study reveals a molecular mechanism regulating increased migratory activity of PMN during cancer progression and suggests a novel therapeutic targeting opportunity.
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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.