ArticleNature communications2022
Pancreatic tumor eradication via selective Pin1 inhibition in cancer-associated fibroblasts and T lymphocytes engagement.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Spatial Multiomics Analyses Reveal That Diabetes Promotes Pancreatic Cancer Progression by Stimulating Cholesterol-Induced Neutrophil Extracellular Trap Formation.Cancer research · 2026Article
- Pre-clinical evaluation of a potent and effective Pin1-degrading agent in pancreatic cancer.Molecular therapy. Oncology · 2025Article
- The Prolyl Isomerase PIN1 Affects Fibroblast Differentiation States and Cross-talk in Pancreatic Cancer.Cancer research · 2025Article
- A polymeric nanovesicle delivers sulfopin and gemcitabine to remodel tumor microenvironment for enhanced chemoimmunotherapy against orthotopic pancreatic cancer.Materials today. Bio · 2025Article
- Synergistic therapy for pancreatic cancer by deactivating cancer-associated fibroblasts and driving T-cell migration into tumor microenvironment using nanochaperone delivery system.Bioactive materials · 2025Article
- Programmable immunoprobiotics orchestrate antitumor immune response with Pin1 inhibition for pancreatic cancer treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Isolation and Ex Vivo Testing of CD8Bio-protocol · 2025Article
- Pin1 as a central node in oncogenic signaling: Mechanistic insights and clinical prospects (Review).Molecular medicine reports · 2025Review
- Drug Delivery System Targeting Cancer-Associated Fibroblast for Improving Immunotherapy.International journal of nanomedicine · 2025Review
- Bilayer 3D co-culture platform inducing the differentiation of normal fibroblasts into cancer-associated fibroblast like cells: New in vitro source to obtain cancer-associated fibroblasts.Bioengineering & translational medicine · 2025Article
- Perineural invasion and the "cold" tumor microenvironment in pancreatic cancer: mechanisms of crosstalk and therapeutic opportunities.Frontiers in immunology · 2025Review
- Nano-strategies targeting cancer-associated fibroblasts to enhance immunotherapy and reverse resistance.Frontiers in immunology · 2025Review
- Fibroblasts as a ruler of the immune microenvironment: measurement and modulation in tissue homeostasis and disease.Frontiers in immunology · 2025Review
- Targeted degradation of Pin1 by protein-destabilizing compounds.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Resveratrol inhibits pancreatic cancer proliferation and metastasis by depleting senescent tumor-associated fibroblasts.World journal of gastrointestinal oncology · 2024Article
- Valence-Change MnOJournal of the American Chemical Society · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Current and future immunotherapeutic approaches in pancreatic cancer treatment.Journal of hematology & oncology · 2024Review
- CAFs-Associated Genes (CAFGs) in Pancreatic Ductal Adenocarcinoma (PDAC) and Novel Therapeutic Strategy.International journal of molecular sciences · 2024Review
- Improving efficacy of TNBC immunotherapy: based on analysis and subtyping of immune microenvironment.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
26 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer associated fibroblasts (CAFs) support tumors via multiple mechanisms, including maintaining the immunosuppressive tumor microenvironment and limiting infiltration of immune cells. The prolyl isomerase Pin1, whose overexpression in CAFs has not been fully profiled yet, plays critical roles in tumor initiation and progression. To decipher effects of selective Pin1 inhibition in CAFs on pancreatic cancer, here we formulate a DNA-barcoded micellular system (DMS) encapsulating the Pin1 inhibitor AG17724. DMS functionalized with CAF-targeting anti-FAP-α antibodies (antiCAFs-DMS) can selectively inhibit Pin1 in CAFs, leading to efficacious but transient tumor growth inhibition. We further integrate DNA aptamers (AptT), which can engage CD8+ T lymphocytes, to obtain a bispecific antiCAFs-DMS-AptT system. AntiCAFs-DMS-AptT inhibits tumor growth in subcutaneous and orthotopic pancreatic cancer models.
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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.