ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
CCN1 Enhances Tumor Immunosuppression through Collagen-Mediated Chemokine Secretion in Pancreatic Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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
10 citing papers in PubMed.
- Renaissance of Traditional Mineral Drugs in Cancer: Advanced Delivery Strategies and Bioengineering Approaches.Pharmaceutics · 2026Review
- Upregulated CCN1 from pleural mesothelial cells alters collagen I conformation and drives fibrosis via ITGB1/MAPK signaling.Cellular & molecular biology letters · 2026Article
- Circulating cellular communication network factor 1 (CCN1) as a liquid biopsy marker indicating progression in advanced melanoma.Journal of translational medicine · 2026Article
- Conditional knockout of Dkk3 drives Lgr5+ progenitor reprogramming into hair cells in the mouse cochlea.Theranostics · 2026Article
- CCN1 as a compartment-specific biomarker of active microenvironmental remodeling: evidence from bone repair, aging, inflammation, and cancer.Frontiers in medicine · 2026Review
- The life cycle of tertiary lymphoid structures in pancreatic cancer-a window of opportunity for immunotherapy.Frontiers in immunology · 2026Review
- The S1PR1-CCN1 axis drives endothelial-to-mesenchymal transition and vascular instability in brain arteriovenous malformations.European journal of medical research · 2025Article
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- CCN1 Enhances Tumor Immunosuppression through Collagen-Mediated Chemokine Secretion in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense, immunosuppressive tumor microenvironment (TME) that limits therapeutic efficacy. This study investigates the role of cellular communication network factor 1 (CCN1, also known as Cyr61), an extracellular matrix-associated protein, in modulating the TME of PDAC. It is demonstrated that Ccn1 promotes PDAC progression by upregulating collagen and chemokine expression, thereby facilitating immune cell exclusion and enhancing tumor growth. Using a Ccn1-deficient PDAC model, decreased collagen and chemokine levels are observed, resulting in increased infiltration of cytotoxic immune cells and reduced myeloid-derived suppressor cells (MDSCs). Furthermore, Ccn1-deficient tumors exhibit heightened sensitivity to gemcitabine and show enhanced responsiveness to anti-programmed cell death 1 (anti-PD1) therapy. Mechanistically, Ccn1 regulates chemokine production through collagen expression, with chemokine levels remaining suppressed even upon interferon-gamma treatment in collagen-deficient cells. These findings highlight Ccn1 as a potential therapeutic target that reprograms the TME to enhance the efficacy of both chemotherapy and immunotherapy in PDAC, providing a novel approach for overcoming immune resistance in PDAC.
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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 Socratic graph.