ArticleOncogene2016
Stromal fibroblasts facilitate cancer cell invasion by a novel invadopodia-independent matrix degradation process.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Gene expression dynamics in fibroblasts during early-stage murine pancreatic carcinogenesis.iScience · 2025Article
- The β-arrestin1/endothelin axis bolsters ovarian fibroblast-dependent invadosome activity and cancer cell metastatic potential.Cell death & disease · 2024Article
- Improving tumor microenvironment assessment in chip systems through next-generation technology integration.Frontiers in bioengineering and biotechnology · 2024Review
- The Cell Biology of Metastatic Invasion in Pancreatic Cancer: Updates and Mechanistic Insights.Cancers · 2023Review
- Cancer-associated fibroblasts: The chief architect in the tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Proteolytic and mechanical remodeling of the extracellular matrix by invadopodia in cancer.Physical biology · 2022Review
- LIS1 interacts with CLIP170 to promote tumor growth and metastasis via the Cdc42 signaling pathway in salivary gland adenoid cystic carcinoma.International journal of oncology · 2022Article
- A novel risk model based on the correlation between the expression of basement membrane genes and immune infiltration to predict the invasiveness of pituitary adenomas.Frontiers in endocrinology · 2022Article
- Cancer-Homing CAR-T Cells and Endogenous Immune Population Dynamics.International journal of molecular sciences · 2021Review
- 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
- Extracellular Matrices and Cancer-Associated Fibroblasts: Targets for Cancer Diagnosis and Therapy?Cancers · 2021Review
- Metastasis-associated fibroblasts: an emerging target for metastatic cancer.Biomarker research · 2021Review
- Synergistic metalloproteinase-based remodeling of matrix by pancreatic tumor and stromal cells.PloS one · 2021Article
- The Cellular Origins of Cancer-Associated Fibroblasts and Their Opposing Contributions to Pancreatic Cancer Growth.Frontiers in cell and developmental biology · 2021Review
- A Complex and Evolutive Character: Two Face Aspects of ECM in Tumor Progression.Frontiers in oncology · 2020Review
- Review
- Tumor-secreted extracellular vesicles promote the activation of cancer-associated fibroblasts via the transfer of microRNA-125b.Journal of extracellular vesicles · 2019Article
- Inhibition of BMI1, a Therapeutic Approach in Endometrial Cancer.Molecular cancer therapeutics · 2018Article
- Chemical Tools for Selective Activity Profiling of Endogenously Expressed MMP-14 in Multicellular Models.ACS chemical biology · 2018Article
- Proteases are Modulated by Fascin in Oral Cancer Invasion.Journal of cancer prevention · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Metastatic invasion of tumors into peripheral tissues is known to rely upon protease-mediated degradation of the surrounding stroma. This remodeling process uses complex, actin-based, specializations of the plasma membrane termed invadopodia that act both to sequester and release matrix metalloproteinases. Here we report that cells of mesenchymal origin, including tumor-associated fibroblasts, degrade substantial amounts of surrounding matrix by a mechanism independent of conventional invadopodia. These degradative sites lack the punctate shape of conventional invadopodia to spread along the cell base and are reticular and/or fibrous in character. In marked contrast to invadopodia, this degradation does not require the action of Src kinase, Cdc42 or Dyn2. Rather, inhibition of Dyn2 causes a marked upregulation of stromal matrix degradation. Further, expression and activity of matrix metalloproteinases are differentially regulated between tumor cells and stromal fibroblasts. This matrix remodeling by fibroblasts increases the invasive capacity of tumor cells, thereby illustrating how the tumor microenvironment can contribute to metastasis. These findings provide evidence for a novel matrix remodeling process conducted by stromal fibroblasts that is substantially more effective than conventional invadopodia, distinct in structural organization and regulated by disparate molecular mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
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.