ArticleNature communications2021
Impairment of a distinct cancer-associated fibroblast population limits tumour growth and metastasis.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 57 citations in OpenAlex.
- Cancer-associated fibroblast subtypes differentially modulate natural killer cells in cancer.Cell reports · 2026Article
- Nanomaterials targeting cancer-associated fibroblasts to overcome stromal barriers in cancer immunotherapy.Journal of nanobiotechnology · 2026Review
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- The Recycling Collagen Receptor uPARAP Is a Unique Mediator of Stromal Drug Delivery to Carcinoma Cells.Molecular cancer therapeutics · 2026Article
- Targeting uPARAP with an Antibody-Drug Conjugate Exhibits Efficacy against Mesothelioma and Synergizes with Cisplatin.Cancer research communications · 2026Article
- Pericytes in hematogenous metastasis: mechanistic insights and therapeutic approaches.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Targeting collagen to optimize cancer immunotherapy.Experimental hematology & oncology · 2025Review
- Article
- Using Cancer-Associated Fibroblasts as a Shear-Wave Elastography Imaging Biomarker to Predict Anti-PD-1 Efficacy of Triple-Negative Breast Cancer.International journal of molecular sciences · 2025Article
- Role of TGFβ-activated cancer-associated fibroblasts in the resistance to checkpoint blockade immunotherapy.Frontiers in oncology · 2025Review
- Cell-cell interactions mediating primary and metastatic breast cancer dormancy.Cancer metastasis reviews · 2024Review
- CAF-Associated Genes in Breast Cancer for Novel Therapeutic Strategies.Biomedicines · 2024Review
- Deciphering the spatial landscape and plasticity of immunosuppressive fibroblasts in breast cancer.Nature communications · 2024Article
- Metabolic targeting of cancer associated fibroblasts overcomes T-cell exclusion and chemoresistance in soft-tissue sarcomas.Nature communications · 2024Article
- Single-cell analysis of immune and stroma cell remodeling in clear cell renal cell carcinoma primary tumors and bone metastatic lesions.Genome medicine · 2024Article
- Single-cell analysis of the cellular landscape of vulvar melanoma provides new insight for immunotherapy administration.BMC cancer · 2024Article
- Generation of 3D Fibroblast-Derived Extracellular Matrix and Analysis of Tumor Cell-Matrix Interactions and Signaling.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Endosialin in Cancer: Expression Patterns, Mechanistic Insights, and Therapeutic Approaches.Theranostics · 2024Review
- Crosstalk between T lymphocyte and extracellular matrix in tumor microenvironment.Frontiers in immunology · 2024Review
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
Profiling studies have revealed considerable phenotypic heterogeneity in cancer-associated fibroblasts (CAFs) present within the tumour microenvironment, however, functional characterisation of different CAF subsets is hampered by the lack of specific markers defining these populations. Here we show that genetic deletion of the Endo180 (MRC2) receptor, predominantly expressed by a population of matrix-remodelling CAFs, profoundly limits tumour growth and metastasis; effects that can be recapitulated in 3D co-culture assays. This impairment results from a CAF-intrinsic contractility defect and reduced CAF viability, which coupled with the lack of phenotype in the normal mouse, demonstrates that upregulated Endo180 expression by a specific, potentially targetable CAF subset is required to generate a supportive tumour microenvironment. Further, characterisation of a tumour subline selected via serial in vivo passage for its ability to overcome these stromal defects provides important insight into, how tumour cells adapt to a non-activated stroma in the early stages of metastatic colonisation.
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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.