ArticleMolecular oncology2014
Collective migration of cancer-associated fibroblasts is enhanced by overexpression of tight junction-associated proteins claudin-11 and occludin.
Article in Molecular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- CCL5 and GLUT1 define leader cells in collective invasion of colorectal cancer.The Journal of pathology · 2026Article
- Emerging agents that target signaling pathways in cancer fibroblast cells (Review).International journal of oncology · 2026Review
- Proteomic signatures of adipocyte recruitment in breast cancer.Endocrine-related cancer · 2026Article
- Interpretable Multimodal Fusion Model for Bridged Histology and Genomics Survival Prediction in Pan-Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Stable and oscillatory hypoxia differentially regulate invasibility of breast cancer associated fibroblasts.Mechanobiology in medicine · 2024Article
- CACNA2D1 regulates the progression and influences the microenvironment of colon cancer.Journal of gastroenterology · 2024Article
- Biophysical perspectives to understanding cancer-associated fibroblasts.APL bioengineering · 2024Review
- Occludin is overexpressed in tubo-ovarian high-grade serous carcinoma compared to mesothelioma and is a marker of tumor progression and chemoresistance.Clinical & experimental metastasis · 2024Article
- Review
- Coordinated reprogramming of renal cancer transcriptome, metabolome and secretome associates with immune tumor infiltration.Cancer cell international · 2023Article
- Autocrine pro-legumain promotes breast cancer metastasis via binding to integrin αvβ3.Oncogene · 2022Article
- Evaluation of the Prognostic Relevance of Differential Claudin Gene Expression Highlights Claudin-4 as Being Suppressed by TGFβ1 Inhibitor in Colorectal Cancer.Frontiers in genetics · 2022Article
- The role of tumor microenvironment and exosomes in dormancy and relapse.Seminars in cancer biology · 2022Review
- Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer.Signal transduction and targeted therapy · 2021Review
- Tumor-Stromal Interactions in a Co-Culture Model of Human Pancreatic Adenocarcinoma Cells and Fibroblasts and Their Connection with Tumor Spread.Biomedicines · 2021Article
- Acquired radioresistance in cancer associated fibroblasts is concomitant with enhanced antioxidant potential and DNA repair capacity.Cell communication and signaling : CCS · 2021Article
- Minimal Residual Disease, Metastasis and Immunity.Biomolecules · 2021Review
- Inhibition of Cathepsin S Restores TGF-β-induced Epithelial-to-mesenchymal Transition and Tight Junction Turnover in Glioblastoma Cells.Journal of Cancer · 2021Article
- Context-Dependent Roles of Claudins in Tumorigenesis.Frontiers in oncology · 2021Review
- Cancer-Associated Fibroblasts Facilitate Squamous Cell Carcinoma Lung Metastasis in Mice by Providing TGFβ-Mediated Cancer Stem Cell Niche.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been suggested that cancer-associated fibroblasts (CAFs) positioned at the desmoplastic areas of various types of cancer are capable of executing a migratory program, characterized by accelerated motility and collective configuration. Since CAFs are reprogrammed derivatives of normal progenitors, including quiescent fibroblasts, we hypothesized that such migratory program could be context-dependent, thus being regulated by specific paracrine signals from the adjacent cancer population. Using the traditional scratch assay setup, we showed that only specific colon cancer cell lines (i.e. HT29) were able to induce collective CAF migration. By performing quantitative proteomics (SILAC), we identified a 2.7-fold increase of claudin-11, a member of the tight junction apparatus, in CAFs that exerted such collectivity in their migratory pattern. Further proteomic investigations of cancer cell line secretomes revealed a specific signature, involving TGF-β, as potential mediator of this effect. Normal colonic fibroblasts stimulated with TGF-β exerted myofibroblastic differentiation, occludin (OCLN) and claudin-11 (CLDN11) overexpression and cohort formation. Subsequently, inhibition of TGF-β attenuated all the previous effects. Immunohistochemistry of the universal tight junction marker occludin in a cohort of 30 colorectal adenocarcinoma patients defined a CAF subpopulation expressing tight junctions. Overall, these data suggest that cancer cells may induce CLDN11 overexpression and subsequent collective migration of peritumoral CAFs via TGF-β secretion.
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