ArticleNature communications2024
The dysadherin/MMP9 axis modifies the extracellular matrix to accelerate colorectal cancer progression.
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 45 papers, 1 of them a synthesis that pooled it.
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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.
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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
45 citing papers in PubMed, 1 synthesis or guideline pooled it.
- From tumor microenvironment orchestrators to actionable targets: a systematic review of TAM-targeted therapies in triple-negative breast cancer.International journal of clinical oncology · 2026Pooled it
- Article
- Integrated Transcriptomic and Proteomic Analysis of the Pathogenic Mechanisms ofAnimals : an open access journal from MDPI · 2026Article
- [Development of a 36-gene signature for predicting recurrence in non-muscle-invasive bladder cancer and validation in a Chinese cohort].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- CD177Gut · 2026Article
- Uncovering ectopic GC-like niches for tumor reactive lymphocyte priming in lung adenocarcinoma using Stereo-XCR-seq.Nature communications · 2026Article
- Cartilage Oligomeric Matrix Protein (COMP) Correlates with Disease Progression, Selected Immune Checkpoint Molecules and SIGLEC9 in Colorectal Cancer.International journal of molecular sciences · 2026Article
- Enhanced expression of ADAMTS1 in ovarian carcinomas: loss of ADAMTS1 expression instigates cellular reprogramming of extracellular matrix ensuing altered plasticity, augmented migration and attenuated adhesion.Journal of biomedical science · 2026Article
- Dehydrocorydaline Exerts Anti-Pancreatic Cancer Effects Through the PI3K/Akt/mTOR Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- ELN orchestrates prometastatic and immunosuppressive niche in bladder cancer via TGFB1 autocrine signaling.JCI insight · 2026Article
- PFAS is associated with perineural invasion in triple-negative breast cancer with a potential role for Cathepsin D dysregulation: a multi-omics and experimental study.Clinical and experimental medicine · 2026Article
- Review
- Review
- Identification of a lactylation-related model for predicting prognosis, tumor-infiltrating immune cells, and chemotherapy response in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Systematic investigation of the potential multi-target pharmacological mechanisms of Astragaloside IV in polycystic ovary syndrome via network pharmacology and in vivo/in vitro experiments.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The dysadherin/carbonic anhydrase 9 axis shapes an acidic tumor microenvironment to promote colorectal cancer progression.Signal transduction and targeted therapy · 2026Article
- Overcoming resistance to anti-PD-1/PD-L1 therapy in cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Article
- Network Pharmacology and Computational Study to Identify Active Components and Potential Targets ofCombinatorial chemistry & high throughput screening · 2026Article
- Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The dynamic alteration of the tumor microenvironment (TME) serves as a driving force behind the progression and metastasis of colorectal cancer (CRC). Within the intricate TME, a pivotal player is the extracellular matrix (ECM), where modifications in components, degradation, and stiffness are considered critical factors in tumor development. In this study, we find that the membrane glycoprotein dysadherin directly targets matrix metalloprotease 9 (MMP9), initiating ECM remodeling within the TME and amplifying cancer progression. Mechanistically, the dysadherin/MMP9 axis not only enhances CRC cell invasiveness and ECM proteolytic activity but also activates cancer-associated fibroblasts, orchestrating the restructuring of the ECM through the synthesis of its components in human CRC cells, patient samples, and mouse models. Notably, disruption of ECM reorganization by dysadherin knockout results in a discernible reduction in the immunosuppressive and proangiogenic milieu in a humanized mouse model. Intriguingly, these effects are reversed upon the overexpression of MMP9, highlighting the intricate and pivotal role of the dysadherin/MMP9 axis in shaping the development of a malignant TME. Therefore, our findings not only highlight that dysadherin contributes to CRC progression by influencing the TME through ECM remodeling but also suggest that dysadherin may be a potential therapeutic target for CRC.
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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.