ArticleThe American journal of pathology2009
Caveolin-1-/- null mammary stromal fibroblasts share characteristics with human breast cancer-associated fibroblasts.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 118 citations in OpenAlex.
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
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- Role of caveolin-1 in metabolic programming of fetal brain.iScience · 2023Article
- Plant extract fromHeliyon · 2023Article
- The complex nature of heterogeneity and its roles in breast cancer biology and therapeutic responsiveness.Frontiers in endocrinology · 2023Review
- MicroRNA-510 mediated negative regulation of Caveolin-1 in fibroblasts promotes aggressive tumor growth.Frontiers in immunology · 2023Article
- Rethinking the biology of metastatic melanoma: a holistic approach.Cancer metastasis reviews · 2021Review
- Reactive Oxygen Species: Do They Play a Role in Adaptive Immunity?Frontiers in immunology · 2021Review
- Cancer-Associated Fibroblasts Regulate Bladder Cancer Invasion and Metabolic Phenotypes through Autophagy.Disease markers · 2021Article
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- Regulation of heterogeneous cancer-associated fibroblasts: the molecular pathology of activated signaling pathways.Journal of experimental & clinical cancer research : CR · 2020Review
- Rab11b-mediated integrin recycling promotes brain metastatic adaptation and outgrowth.Nature communications · 2020Article
- Fibroblast subtypes define a metastatic matrisome in breast cancer.JCI insight · 2020Article
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- The roles of glucose metabolic reprogramming in chemo- and radio-resistance.Journal of experimental & clinical cancer research : CR · 2019Review
- The combined expressions of B7H4 and ACOT4 in cancer-associated fibroblasts are related to poor prognosis in patients with gastric carcinoma.International journal of clinical and experimental pathology · 2019Article
- A peek into cancer-associated fibroblasts: origins, functions and translational impact.Disease models & mechanisms · 2018Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 3 institutions in 4 countries.
Funding
Abstract
Recently, we reported that human breast cancer-associated fibroblasts show functional inactivation of the retinoblastoma (RB) tumor suppressor and down-regulation of caveolin-1 (Cav-1) protein expression. However, it remains unknown whether loss of Cav-1 is sufficient to confer functional RB inactivation in mammary fibroblasts. To establish a direct cause-and-effect relationship, mammary stromal fibroblasts (MSFs) were prepared from Cav-1(-/-) null mice and subjected to phenotypic analysis. Here, we provide evidence that Cav-1(-/-) MSFs share many characteristics with human cancer-associated fibroblasts. The Cav-1(-/-) MSF transcriptome significantly overlaps with human cancer-associated fibroblasts; both show a nearly identical profile of RB/E2F-regulated genes that are up-regulated, which is consistent with RB inactivation. This Cav-1(-/-) MSF gene signature is predictive of poor clinical outcome in breast cancer patients treated with tamoxifen. Consistent with these findings, Cav-1(-/-) MSFs show RB hyperphosphorylation and the up-regulation of estrogen receptor co-activator genes. We also evaluated the paracrine effects of "conditioned media" prepared from Cav-1(-/-) MSFs on wild-type mammary epithelia. Our results indicate that Cav-1(-/-) MSF "conditioned media" is sufficient to induce an epithelial-mesenchymal transition, indicative of an invasive phenotype. Proteomic analysis of this "conditioned media" reveals increased levels of proliferative/angiogenic growth factors. Consistent with these findings, Cav-1(-/-) MSFs are able to undergo endothelial-like transdifferentiation. Thus, these results have important implications for understanding the role of cancer-associated fibroblasts and RB inactivation in promoting tumor angiogenesis.
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