ArticleJournal of the Royal Society, Interface2019
Collagen content and extracellular matrix cause cytoskeletal remodelling in pancreatic fibroblasts.
Article in Journal of the Royal Society, Interface, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Atomic force microscopy-based nanomechanical signatures as cancer biomarkers in a nutshell.FEBS letters · 2026Review
- Radiation-Induced Alterations in Cancer-Associated Fibroblasts: Drivers of Tumor Radioresistance and Therapeutic Targets.Biomolecules · 2026Review
- Cancer cells metastasize in several types of cancer via two distinct routes, probably based on mechanical signals.Frontiers in cell and developmental biology · 2026Review
- The type I collagen paradox in PDAC progression: microenvironmental protector turned tumor accomplice.Journal of translational medicine · 2025Review
- Viscosity regulates cell spreading and cell-extracellular matrix interactions.The FEBS journal · 2025Article
- The mechanopathology of the tumor microenvironment: detection techniques, molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
- Biophysical perspectives to understanding cancer-associated fibroblasts.APL bioengineering · 2024Review
- Review
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Oncogene · 2024Article
- Toward innovative approaches for exploring the mechanically regulated tumor-immune microenvironment.APL bioengineering · 2024Review
- Identification of key genes associated with endometriosis and endometrial cancer by bioinformatics analysis.Frontiers in oncology · 2024Article
- Multilevel Assessment of Stent-Induced Inflammation in the Adjacent Vascular Tissue.ACS biomaterials science & engineering · 2023Article
- YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression.Research square · 2023Article
- Fascin-1 in Cancer Cell Metastasis: Old Target-New Insights.International journal of molecular sciences · 2023Review
- Pancreatic Cancer Presents Distinct Nanomechanical Properties During Progression.Annals of biomedical engineering · 2023Article
- Insights in Cell Biomechanics through Atomic Force Microscopy.Materials (Basel, Switzerland) · 2023Review
- Unravelling cell migration: defining movement from the cell surface.Cell adhesion & migration · 2022Review
- Contribution of mechanical homeostasis to epithelial-mesenchymal transition.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Collagen Remodeling along Cancer Progression Providing a Novel Opportunity for Cancer Diagnosis and Treatment.International journal of molecular sciences · 2022Review
- Modeling Pancreatic Cancer with Patient-Derived Organoids Integrating Cancer-Associated Fibroblasts.Cancers · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In many solid tumours a desmoplastic reaction takes place, which results in tumour tissue stiffening due to the extensive production of extracellular matrix (ECM) proteins, such as collagen, by stromal cells, mainly fibroblasts (FBs) and cancer-associated fibroblasts (CAFs). In this study, we investigated the effect of collagen stiffness on pancreatic FBs and CAFs, particularly on specific cytoskeleton properties and gene expression involved in tumour invasion. We found that cells become stiffer when they are cultured on stiff substrates and express higher levels of alpha-smooth muscle actin (α-SMA). Also, it was confirmed that on stiff substrates, CAFs are softer than FBs, while on soft substrates they have comparable Young's moduli. Furthermore, the number of spread FBs and CAFs was higher in stiffer substrates, which was also confirmed by Ras-related C3 botulinum toxin substrate 1 ( RAC1) mRNA expression, which mediates cell spreading. Although stress fibres in FBs become more oriented on stiff substrates, CAFs have oriented stress fibres regardless of substrate stiffness. Subsequently, we demonstrated that cells' invasion has a differential response to stiffness, which was associated with regulation of Ras homologue family member ( RhoA) and Rho-associated, coiled-coil containing protein kinase 1 ( ROCK-1) mRNA expression. Overall, our results demonstrate that collagen stiffness modulates FBs and CAFs cytoskeleton remodelling and alters their invasion properties.
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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.