ArticleNature communications2022
Cancer cell survival depends on collagen uptake into tumor-associated stroma.
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 42 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
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Who cites it
42 citing papers in PubMed, 59 citations in OpenAlex.
- Collagen-Binding IL-15 Immunocytokine Armed Oncolytic Adenovirus Establishes a Self-Reinforcing Immunostimulatory Milieu to Potentiate Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Beyond the scaffold: extracellular matrix uptake in breast cancer.Biochemical Society transactions · 2026Review
- Proteomic analysis of malignant ascites and its impact on ovarian cancer spheroids.Clinical proteomics · 2026Article
- Decoupling Mechanical Confinement and Fibrotic Extracellular Matrix Signaling in Vestibular Schwannoma Using Tunable 3D Hydrogels.Cellular and molecular bioengineering · 2026Article
- ECM (collagen) mediated signaling drives the emergence of androgen independence in prostate cancer cells.Biochemistry and biophysics reports · 2026Article
- Overview of glutamine metabolism in stromal components of the tumor microenvironment and potential anti-tumor therapies.Genes & diseases · 2026Review
- Identification of COL4A2 as a Biomarker of Extracellular Matrix Remodeling and Vascular Scaffold in Choroid for Myopia.Investigative ophthalmology & visual science · 2026Article
- A block staining method using ethanolic phosphotungstic acid for the visualisation of collagens in transmission electron microscopy.PloS one · 2026Article
- Harnessing SARS-CoV-2 immunity to promote antitumor responses through intratumoral vaccination and adoptive transfer.Frontiers in immunology · 2026Article
- GPR4 promotes immune exclusion in colon cancer through LOXL2-mediated extracellular matrix remodeling.Nature communications · 2025Article
- The role of hyperthermia in modern radiation treatment- state of art.Radiation oncology (London, England) · 2025Review
- BRD4 inhibition sensitizes glioblastoma to radiotherapy by suppressing super-enhancer-driven COL1A1.Oncogene · 2025Article
- Mitochondrial morphological aberrations and redistribution in podocytes with glomerular diseases.Renal failure · 2025Article
- Collagen dynamics in the breast cancer tumor microenvironment and therapeutic perspectives.Discover oncology · 2025Review
- A 3D Bioprinted Pancreatic Cancer Model Using Collagen-Gelatin Methacrylamide-Alginate Bioinks to Mimic the Desmoplastic Microenvironment.Biomacromolecules · 2025Article
- Cancer-Associated Fibroblasts: Origin, Classification, Tumorigenicity, and Targeting for Cancer Therapy.MedComm · 2025Review
- ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.Nature cardiovascular research · 2025Article
- Waging war against cardiac fibrosis by targeting the anthrax toxin receptor.Nature cardiovascular research · 2025Article
- Collagen in pituitary adenomas: A comprehensive review of biological roles and clinical implications.Journal of clinical & translational endocrinology · 2025Review
- NC410, a bivalent LAIR-2 construct, remodels collagen in the tumor microenvironment and abrogates neutrophil-driven T cell suppression.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
Corrections and comments
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Authors and funding
22 authors at 10 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Collagen I, the most abundant protein in humans, is ubiquitous in solid tumors where it provides a rich source of exploitable metabolic fuel for cancer cells. While tumor cells were unable to exploit collagen directly, here we show they can usurp metabolic byproducts of collagen-consuming tumor-associated stroma. Using genetically engineered mouse models, we discovered that solid tumor growth depends upon collagen binding and uptake mediated by the TEM8/ANTXR1 cell surface protein in tumor-associated stroma. Tumor-associated stromal cells processed collagen into glutamine, which was then released and internalized by cancer cells. Under chronic nutrient starvation, a condition driven by the high metabolic demand of tumors, cancer cells exploited glutamine to survive, an effect that could be reversed by blocking collagen uptake with TEM8 neutralizing antibodies. These studies reveal that cancer cells exploit collagen-consuming stromal cells for survival, exposing an important vulnerability across solid tumors with implications for developing improved anticancer therapy.
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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.