ArticleBiophysical journal2015
Palladin mediates stiffness-induced fibroblast activation in the tumor microenvironment.
Article in Biophysical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- 3DACS biomaterials science & engineering · 2023Pooled it
- Pulsed Low-Dose-Rate Chemoradiation Induces Stromal Reprogramming in Pancreatic CAF-Generated ECM: Quantification by the HOST-Factor.Gastro hep advances · 2026Article
- PeriostinBone research · 2024Article
- Macrophages and fibroblasts in foreign body reactions: How mechanical cues drive cell functions?Materials today. Bio · 2023Review
- Biophysics involved in the process of tumor immune escape.iScience · 2022Review
- Integrated Quantitative Phosphoproteomics and Cell-based Functional Screening Reveals Specific Pathological Cardiac Hypertrophy-related Phosphorylation Sites.Molecules and cells · 2021Article
- Proteinaceous Hydrogels for Bioengineering Advanced 3D Tumor Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Review
- Human Adventitial Fibroblast Phenotype Depends on the Progression of Changes in Substrate Stiffness.Advanced healthcare materials · 2020Article
- The MyMOMA domain of MYO19 encodes for distinct Miro-dependent and Miro-independent mechanisms of interaction with mitochondrial membranes.Cytoskeleton (Hoboken, N.J.) · 2020Article
- Expression quantitative trait loci for PI3K/AKT pathway.Medicine · 2017Article
- Stiffened Extracellular Matrix and Signaling from Stromal Fibroblasts via Osteoprotegerin Regulate Tumor Cell Invasion in a 3-D Tumor in Situ Model.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2016Article
- Twist1-induced activation of human fibroblasts promotes matrix stiffness by upregulating palladin and collagen α1(VI).Oncogene · 2016Article
- Stromal dynamic reciprocity in cancer: intricacies of fibroblastic-ECM interactions.Current opinion in cell biology · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical properties of the tumor microenvironment have emerged as key factors in tumor progression. It has been proposed that increased tissue stiffness can transform stromal fibroblasts into carcinoma-associated fibroblasts. However, it is unclear whether the three to five times increase in stiffness seen in tumor-adjacent stroma is sufficient for fibroblast activation. In this study we developed a three-dimensional (3D) hydrogel model with precisely tunable stiffness and show that a physiologically relevant increase in stiffness is sufficient to lead to fibroblast activation. We found that soluble factors including CC-motif chemokine ligand (CCL) chemokines and fibronectin are necessary for this activation, and the combination of C-C chemokine receptor type 4 (CCR4) chemokine receptors and β1 and β3 integrins are necessary to transduce these chemomechanical signals. We then show that these chemomechanical signals lead to the gene expression changes associated with fibroblast activation via a network of intracellular signaling pathways that include focal adhesion kinase (FAK) and phosphoinositide 3-kinase (PI3K). Finally, we identify the actin-associated protein palladin as a key node in these signaling pathways that result in fibroblast activation.
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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.