ArticleThe Journal of experimental medicine2021
Matrix compliance permits NF-κB activation to drive therapy resistance in breast cancer.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 60 citations in OpenAlex.
- Mechanosensors Collaborate to Regulate DNA Damage Repair in Hepatocellular Carcinoma.Cancer research · 2026Article
- Organoids in Precision Radiotherapy: Methodological Foundations, Tumor-Specific Evidence, and Translational Roadmaps.Cancer medicine · 2026Review
- Notch1 O-GlcNAcylation drives tumor stemness and mechanoadaptation to a stiff microenvironment and promotes chordoma recurrence.The Journal of clinical investigation · 2026Article
- Increased Toll-Like Receptor-4 Signalling in Breast Tissue of High Fibroglandular Density.Journal of mammary gland biology and neoplasia · 2026Article
- Dynamic hydrogel mechanics in organoid engineering: From matrix design to translational paradigms.Bioactive materials · 2026Review
- Three-dimensional-bioprinted stiff matrix triggers PDAC radioresistance through histone H3 lysine 18 lactylation (H3K18la) potentiates RAD51 activation.Regenerative biomaterials · 2026Article
- Exploring the Role of Long Noncoding RNAs in Breast Cancer Progression: A Comprehensive Study on Biomarkers and Therapeutic Approaches.Cancer medicine · 2026Review
- BRD4 inhibition sensitizes glioblastoma to radiotherapy by suppressing super-enhancer-driven COL1A1.Oncogene · 2025Article
- Myosin-actin pattern links matrix stiffness to GFAT2-hyaluronan metabolism.Materials today. Bio · 2025Article
- Mechanism of ECM Stiffness-Integrin-Hippo-ABCG1 axis in regulating ferroptosis and targeted nanodrug intervention in LUAD.Respiratory research · 2025Article
- Tumor microenvironment response to neoadjuvant therapy in breast cancer: insights from single-cell and spatial omics.Medical oncology (Northwood, London, England) · 2025Review
- Tissue mechanics in tumor heterogeneity and aggression.Trends in cancer · 2025Review
- Radiation-guided nanoparticles enhance the efficacy of PARP inhibitors in primary and metastatic BRCA1-deficient tumors via immunotherapy.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Extracellular matrix stiffness: mechanisms in tumor progression and therapeutic potential in cancer.Experimental hematology & oncology · 2025Review
- Effects of hydrogel stiffness and viscoelasticity on organoid culture: a comprehensive review.Molecular medicine (Cambridge, Mass.) · 2025Review
- Forcing the code: tension modulates signaling to drive morphogenesis and malignancy.Genes & development · 2025Review
- Extracellular Matrix Stiffness Enhancement Promotes Docetaxel Resistance in Prostate Cancer via Inhibition of Apoptosis Mediated by Upregulation of PRRX1.International journal of medical sciences · 2025Article
- Understanding cellular proliferation activity in breast cancer using multi-compartment model of transverse relaxation time mapping on 3T MRI.Frontiers in oncology · 2025Article
- Exploiting Matrix Stiffness to Overcome Drug Resistance.ACS biomaterials science & engineering · 2024Review
- Pioglitazone enhances cisplatin's impact on triple-negative breast cancer: Role of PPARγ in cell apoptosis.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Triple-negative breast cancers (TNBCs) are associated with poor survival mediated by treatment resistance. TNBCs are fibrotic, yet little is known regarding how the extracellular matrix (ECM) evolves following therapy and whether it impacts treatment response. Analysis revealed that while primary untreated TNBCs are surrounded by a rigid stromal microenvironment, chemotherapy-resistant residual tumors inhabit a softer niche. TNBC organoid cultures and xenograft studies showed that organoids interacting with soft ECM exhibit striking resistance to chemotherapy, ionizing radiation, and death receptor ligand TRAIL. A stiff ECM enhanced proapoptotic JNK activity to sensitize cells to treatment, whereas a soft ECM promoted treatment resistance by elevating NF-κB activity and compromising JNK activity. Treatment-resistant residual TNBCs residing within soft stroma had elevated activated NF-κB levels, and disengaging NF-κB activity sensitized tumors in a soft matrix to therapy. Thus, the biophysical properties of the ECM modify treatment response, and agents that modulate stiffness-dependent NF-κB or JNK activity could enhance therapeutic efficacy in patients with TNBC.
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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.