ArticleNature communications2024
Macrophage-fibroblast JAK/STAT dependent crosstalk promotes liver metastatic outgrowth in pancreatic cancer.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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
56 citing papers in PubMed, 61 citations in OpenAlex.
- Article
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- Immune-stromal interactions at the crossroads of tissue injury, repair, and tumor progression.Med (New York, N.Y.) · 2026Review
- Chlorin e6-mediated sublethal photodynamic therapy modulates biomarkers in a murine lung cancer-derived in vitro cancer-associated fibroblast model.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Macrophage-Derived Extracellular Vesicles Deliver Progranulin to Alleviate Skin Wound Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- 25 Years of Cancer Immunoediting: Dendritic Cells and Macrophages Filled the Missing Gap.Cancers · 2026Review
- Molecular phenotypes and spatial archetypes: A new framework for cancer-associated fibroblasts.Cancer cell · 2026Review
- Review
- Immune-driven stromal inflammation in pancreatic cancer within a microfluidic platform.Biofabrication · 2026Article
- Extracellular vesicles from chemotherapy-induced senescent tumor cells reprogram hepatic phospholipid metabolism to promote pancreatic cancer liver metastasis.Journal of experimental & clinical cancer research : CR · 2026Article
- Macrophage Extracellular Traps in the Oral Mucosa: Autoimmune Disease and Platelet-Derived Epithelial Modulation.Life (Basel, Switzerland) · 2026Article
- Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity.Current oncology reports · 2026Review
- High-Dimensional Protein Analysis Uncovers Distinct Immunologic and Stromal Features in Primary and Metastatic Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- miR-500a-3p negatively regulates SOCS2 and participates in the proliferation, glycolysis, and apoptosis of HCC cells via the JAK2/STAT5 pathway.Journal of applied biomedicine · 2026Article
- The research advances of crosstalk between cancer-associated fibroblasts and tumor cells using co-culture organoids.Cell death & disease · 2026Review
- MacrophageJournal for immunotherapy of cancer · 2026Article
- Palmaturbine Inhibits Pancreatic Ductal Adenocarcinoma by Suppressing the JAK2/STAT3 Signaling Pathway.International journal of molecular sciences · 2026Article
- The Significance of the Heterogeneity of Cancer-Associated Fibroblasts in Tumor Microenvironments.Metabolites · 2026Review
- Progranulin impairs efferocytosis of macrophages in renal fibrosis by negatively regulating PPAR-δ-mediated inhibition of the JAK-STAT signaling pathway.Cellular and molecular life sciences : CMLS · 2026Article
- Targeting metabolic-epigenetic-immune axis in cancer: molecular mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2026Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic disease for which better therapies are urgently needed. Fibroblasts and macrophages are heterogeneous cell populations able to enhance metastasis, but the role of a macrophage-fibroblast crosstalk in regulating their pro-metastatic functions remains poorly understood. Here we deconvolve how macrophages regulate metastasis-associated fibroblast (MAF) heterogeneity in the liver. We identify three functionally distinct MAF populations, among which the generation of pro-metastatic and immunoregulatory myofibroblastic-MAFs (myMAFs) critically depends on macrophages. Mechanistically, myMAFs are induced through a STAT3-dependent mechanism driven by macrophage-derived progranulin and cancer cell-secreted leukaemia inhibitory factor (LIF). In a reciprocal manner, myMAF secreted osteopontin promotes an immunosuppressive macrophage phenotype resulting in the inhibition of cytotoxic T cell functions. Pharmacological blockade of STAT3 or myMAF-specific genetic depletion of STAT3 restores an anti-tumour immune response and reduces metastases. Our findings provide molecular insights into the complex macrophage-fibroblast interactions in tumours and reveal potential targets to inhibit PDAC liver metastasis.
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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.