ArticleNature communications2021
Co-evolution of matrisome and adaptive adhesion dynamics drives ovarian cancer chemoresistance.
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 110 papers, 1 of them a synthesis that pooled it.
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Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.
- Overlapping gene dependencies for PARP inhibitors and carboplatin response identified by functional CRISPR-Cas9 screening in ovarian cancer.Cell death & disease · 2022Pooled it
- Understanding and targeting the tumour matrisome.Nature reviews. Clinical oncology · 2026Review
- Tumor FAK supports fibrillar collagen expression in ovarian cancer ascites.Matrix biology : journal of the International Society for Matrix Biology · 2026Article
- Epithelial-mesenchymal transition in carcinoma: navigating phenotypic states to target resistance and metastasis.Cancer metastasis reviews · 2026Review
- Exosome-Associated Proteins as Mediators and Biomarkers of Ovarian Cancer Dissemination.Biomolecules · 2026Review
- RelB drives integrin-mediated stress tolerance and relapse in high-grade serous ovarian cancer.Cell reports · 2026Article
- Tumor evolution: signaling pathways, molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Drug resistant cancer cells show increased nuclear mechanotransduction and mechanically targetable YAP-regulated vulnerability.Biomaterials · 2026Article
- Oxidative Stress and Antioxidant Defense Mechanisms inAntioxidants (Basel, Switzerland) · 2026Article
- Unmasking the common enemy: drug resistance mechanisms across three different EGFR inhibitor generations are associated with co-targetable alterations in extracellular matrix signaling.Cell communication and signaling : CCS · 2026Article
- Cross-assay RNA modeling reveals cancer biomarkers.bioRxiv : the preprint server for biology · 2026Article
- Disarming cancer resistance: FAK as a therapeutic target.Trends in cancer · 2026Review
- Mapping immunosuppressive terrain in high-grade serous ovarian cancer: tumor-intrinsic, stromal, and spatial drivers of therapy response.NPJ precision oncology · 2026Review
- Matrix structure and microenvironment dynamics correlate with chemotherapy response in ovarian cancer.iScience · 2026Article
- Extracellular matrix polysaccharides and glycoproteins in ovarian cancer: structural-functional macromolecular perspectives and potential exosome-derived biomarkers.Cell communication and signaling : CCS · 2026Review
- Cell-intrinsic and tumor microenvironmental determinants of platinum resistance in epithelial ovarian cancer.Discover oncology · 2026Review
- Normalizing the Tumor Microenvironment: A New Frontier in Ovarian Cancer Therapy.International journal of molecular sciences · 2026Review
- Comparative proteomic analysis of the ECM composition of the human omentum and mesentery, the main sites of ovarian cancer metastasis.iScience · 2026Article
- New insight into the risk stratification and treatment priority of breast cancer: TMT scoring system.International journal of surgery (London, England) · 2026Article
- A prognostic matrix gene expression signature defines functional glioblastoma phenotypes and niches.Communications biology · 2026Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to its dynamic nature, the evolution of cancer cell-extracellular matrix (ECM) crosstalk, critically affecting metastasis and treatment resistance, remains elusive. Our results show that platinum-chemotherapy itself enhances resistance by progressively changing the cancer cell-intrinsic adhesion signaling and cell-surrounding ECM. Examining ovarian high-grade serous carcinoma (HGSC) transcriptome and histology, we describe the fibrotic ECM heterogeneity at primary tumors and distinct metastatic sites, prior and after chemotherapy. Using cell models from systematic ECM screen to collagen-based 2D and 3D cultures, we demonstrate that both specific ECM substrates and stiffness increase resistance to platinum-mediated, apoptosis-inducing DNA damage via FAK and β1 integrin-pMLC-YAP signaling. Among such substrates around metastatic HGSCs, COL6 was upregulated by chemotherapy and enhanced the resistance of relapse, but not treatment-naïve, HGSC organoids. These results identify matrix adhesion as an adaptive response, driving HGSC aggressiveness via co-evolving ECM composition and sensing, suggesting stromal and tumor strategies for ECM pathway targeting.
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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.