ArticleNature communications2025
Targeting spermine metabolism to overcome immunotherapy resistance in pancreatic cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Arginine metabolism, polyamine homeostasis and ferroptosis in cancer: Molecular links and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- Stimuli-responsive structural transformation of adaptive peptide nanomaterials toward biomedical applications.Materials today. Bio · 2026Review
- CLCA1 as an immune prognostic biomarker and therapeutic target in colorectal cancer.Translational cancer research · 2026Article
- RBX1Cancers · 2026Article
- Construction of a SEMA3 family-based model to predict prognosis and molecular subtypes in pancreatic ductal adenocarcinoma.Discover oncology · 2026Article
- Gut microbiota-host adaptive immune interactions in type 2 diabetes mellitus: mechanisms, disease progression, and microbiota-based therapeutic strategies.Frontiers in microbiology · 2026Review
- GJB5 expression in pancreatic adenocarcinoma: prognostic significance and therapeutic implications.American journal of translational research · 2026Article
- Spermine synthase in Snyder-Robinson syndrome and cancer.Molecular biology reports · 2025Review
- Therapeutic cancer vaccines in pancreatic cancer.Frontiers in immunology · 2025Review
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Authors and funding
22 authors.
Funding
Abstract
While dysregulation of polyamine metabolism is frequently observed in cancer, it is unknown how polyamines alter the tumor microenvironment (TME) and contribute to therapeutic resistance. Analysis of polyamines in the plasma of pancreatic cancer patients reveals that spermine levels are significantly elevated and correlate with poor prognosis. Using a multi-omics approach, we identify Serpinb9 as a vulnerability in spermine metabolism in pancreatic cancer. Serpinb9, a serine protease inhibitor, directly interacts with spermine synthase (SMS), impeding its lysosome-mediated degradation and thereby augmenting spermine production and secretion. Mechanistically, the accumulation of spermine in the TME alters the metabolic landscape of immune cells, promoting CD8
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