ArticleNature communications2020
Heat Shock Factor 1-dependent extracellular matrix remodeling mediates the transition from chronic intestinal inflammation to colon cancer.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 102 citations in OpenAlex.
- Adaptation to heat stress by diversification of the vertebrate heat shock transcription factor family.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Heat shock transcription factor 1 acts as an endogenous protective mechanism in mechanically stretched alveolar epithelial cells.Cell stress & chaperones · 2026Article
- Paired mutation calling and spatial transcriptomics identify cellular neighborhoods associated with the neoplastic outcome of mouse colitis.Nature genetics · 2026Article
- Heat shock transcription factors in development and disease.Disease models & mechanisms · 2026Review
- Dendritic cell-liposome conjugates reverse immunosuppressive tumor microenvironment for inhibiting colitis-associated colorectal cancer.Acta pharmacologica Sinica · 2026Article
- DANEELpath open source digital analysis tools for histopathological research in neuroblastoma models.Scientific reports · 2026Article
- Exploratory transcriptomic analysis of mouse articular cartilage in response to tissue inhibitor of metalloproteinase 3 identifies inflammation-associated gene expression changes.Frontiers in immunology · 2026Article
- The role of extracellular matrix stiffness in regulating fibroblast behaviors and disease progression.Frontiers in immunology · 2026Review
- Conservation of mRNA operon formation in control of the heat shock response in mammalian cells.Science advances · 2025Article
- The immune microenvironment of colorectal cancer.Nature reviews. Cancer · 2025Review
- Human intestinal fungus Clavispora lusitaniae attenuates colitis through Pyruvate decarboxylase-derived Indole-3-ethanol.Nature communications · 2025Article
- HSF1-DBC1 axis drives prostate cancer progression by activating a metastatic transcriptional program.Experimental & molecular medicine · 2025Article
- A guide to heat shock factors as multifunctional transcriptional regulators.The FEBS journal · 2025Review
- Tianma Granules Alleviate AOM/DSS-Induced Colorectal Tumorigenesis by Inhibiting the Wnt/β-Catenin Pathway Activation.Journal of cellular and molecular medicine · 2025Article
- Identification of Cancer Associated Fibroblasts Related Genes Signature to Facilitate Improved Prediction of Prognosis and Responses to Therapy in Patients with Pancreatic Cancer.International journal of molecular sciences · 2025Article
- Multi-omics perspective: mechanisms of gastrointestinal injury repair.Burns & trauma · 2025Review
- 3-O-Acetyl-11-Keto-Oncology research · 2025Article
- Article
- CAF-induced physical constraints controlling T cell state and localization in solid tumours.Nature reviews. Cancer · 2024Review
- A New Combination ofFoods (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
In the colon, long-term exposure to chronic inflammation drives colitis-associated colon cancer (CAC) in patients with inflammatory bowel disease. While the causal and clinical links are well established, molecular understanding of how chronic inflammation leads to the development of colon cancer is lacking. Here we deconstruct the evolving microenvironment of CAC by measuring proteomic changes and extracellular matrix (ECM) organization over time in a mouse model of CAC. We detect early changes in ECM structure and composition, and report a crucial role for the transcriptional regulator heat shock factor 1 (HSF1) in orchestrating these events. Loss of HSF1 abrogates ECM assembly by colon fibroblasts in cell-culture, prevents inflammation-induced ECM remodeling in mice and inhibits progression to CAC. Establishing relevance to human disease, we find high activation of stromal HSF1 in CAC patients, and detect the HSF1-dependent proteomic ECM signature in human colorectal cancer. Thus, HSF1-dependent ECM remodeling plays a crucial role in mediating inflammation-driven colon cancer.
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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.