ArticlePloS one2019
Reciprocal signaling and direct physical interactions between fibroblasts and breast cancer cells in a 3D environment.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Minimal Residual Disease in Breast Cancer: Tumour Microenvironment Interactions, Detection Methods and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- In vitro detection of cancer cells using a novel fluorescent choline derivative.BMC medical imaging · 2024Article
- Evaluation of Targeted Alpha Therapy Using [International journal of molecular sciences · 2024Article
- Extracellular vesicle depletion and UGCG overexpression mitigate the cell density effect in HEK293 cell culture transfection.Molecular therapy. Methods & clinical development · 2024Article
- Modelling the complex nature of the tumor microenvironment: 3D tumor spheroids as an evolving tool.Journal of biomedical science · 2024Review
- Exploring the multifaceted role of direct interaction between cancer cells and fibroblasts in cancer progression.Frontiers in molecular biosciences · 2024Review
- Crosstalk with lung fibroblasts shapes the growth and therapeutic response of mesothelioma cells.Cell death & disease · 2023Article
- Recent advances in 3D bioprinted tumor models for personalized medicine.Translational oncology · 2023Article
- The role of cancer-associated fibroblasts in breast cancer metastasis.Frontiers in oncology · 2023Review
- Triple-negative and triple-positive breast cancer cells reciprocally control their growth and migration via the S100A4 pathway.Cell adhesion & migration · 2022Article
- Multiple Cell Cultures for MRI Analysis.International journal of molecular sciences · 2022Review
- Maintaining Myofibroblastic-Like Cancer-Associated Fibroblasts by Cancer Stemness Signal Transduction Feedback Loop.Cureus · 2022Article
- Implications for Immunotherapy of Breast Cancer by Understanding the Microenvironment of a Solid Tumor.Cancers · 2022Review
- Modulation of peritumoral fibroblasts with a membrane-tethered tissue inhibitor of metalloproteinase (TIMP) for the elimination of cancer cells.Investigational new drugs · 2022Article
- 3D and 4D Tumorigenesis Model for the Quantitative Analysis of Cancer Cell Behavior and Screening for Anticancer Drugs.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Directed movement toward, translocation along, penetration into and exit from vascular networks by breast cancer cells in 3D.Cell adhesion & migration · 2021Article
- Development of a model for fibroblast-led collective migration from breast cancer cell spheroids to study radiation effects on invasiveness.Radiation oncology (London, England) · 2021Article
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- Breast cancer-associated skeletal muscle mitochondrial dysfunction and lipid accumulation is reversed by PPARG.American journal of physiology. Cell physiology · 2021Article
- Article
Corrections and comments
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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
Tumorigenic cells undergo cell aggregation and aggregate coalescence in a 3D Matrigel environment. Here, we expanded this 3D platform to assess the interactions of normal human dermal fibroblasts (NHDFs) and human primary mammary fibroblasts (HPMFs) with breast cancer-derived, tumorigenic cells (MDA-MB-231). Medium conditioned by MDA-MB-231 cells activates both types of fibroblasts, imbuing them with the capacity to accelerate the rate of aggregation and coalescence of MDA-MB-231 cells more than four fold. Acceleration is achieved 1) by direct physical interactions with MDA-MB-231 cells, in which activated fibroblasts penetrate the MDA-MB-231/Matrigel 3D environment and function as supporting scaffolds for MDA-MB-231 aggregation and coalescence, and 2) through the release of soluble accelerating factors, including matrix metalloproteinase (MMPs) and, in the case of activated NHDFs, SDF-1α/CXCL12. Fibroblast activation includes changes in morphology, motility, and gene expression. Podoplanin (PDPN) and fibroblast activation protein (FAP) are upregulated by more than nine-fold in activated NHDFs while activated HPMFs upregulate FAP, vimentin, desmin, platelet derived growth factor receptor A and S100A4. Overexpression of PDPN, but not FAP, in NHDF cells in the absence of MDA-MB-231-conditioned medium, activates NHDFs. These results reveal that complex reciprocal signaling between fibroblasts and cancer cells, coupled with their physical interactions, occurs in a highly coordinated fashion that orchestrates aggregation and coalescence, behaviors specific to cancer cells in a 3D environment. These in vitro interactions may reflect events involved in early tumorigenesis, particularly in cases of field cancerization, and may represent a new mechanism whereby cancer-associated fibroblasts (CAFs) promote tumor growth.
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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 Socratic graph.