ArticleThe American journal of pathology2006
Caveolin-1 deficiency (-/-) conveys premalignant alterations in mammary epithelia, with abnormal lumen formation, growth factor independence, and cell invasiveness.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Behind Brain Metastases Formation: Cellular and Molecular Alterations and Blood-Brain Barrier Disruption.International journal of molecular sciences · 2021Article
- Caveolin-1 enhances brain metastasis of non-small cell lung cancer, potentially in association with the epithelial-mesenchymal transition marker SNAIL.Cancer cell international · 2019Article
- Pathway‑based detection of idiopathic pulmonary fibrosis at an early stage.Molecular medicine reports · 2017Article
- Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy.Autophagy · 2015Article
- Value of caveolin-1 in cancer progression and prognosis: Emphasis on cancer-associated fibroblasts, human cancer cells and mechanism of caveolin-1 expression (Review).Oncology letters · 2014Article
- The retinoblastoma tumor suppressor pathway modulates the invasiveness of ErbB2-positive breast cancer.Oncogene · 2014Article
- Model cell membranes: Techniques to form complex biomimetic supported lipid bilayers via vesicle fusion.Current opinion in colloid & interface science · 2013Article
- Divergent control of Cav-1 expression in non-cancerous Li-Fraumeni syndrome and human cancer cell lines.Cancer biology & therapy · 2013Article
- Article
- Caveolin-1 is related to invasion, survival, and poor prognosis in hepatocellular cancer.Medical oncology (Northwood, London, England) · 2012Article
- Caveolin-1 promotes pancreatic cancer cell differentiation and restores membranous E-cadherin via suppression of the epithelial-mesenchymal transition.Cell cycle (Georgetown, Tex.) · 2011Article
- Signal transducer and activator of transcription 5 as a key signaling pathway in normal mammary gland developmental biology and breast cancer.Breast cancer research : BCR · 2011Review
- Neuron-targeted caveolin-1 protein enhances signaling and promotes arborization of primary neurons.The Journal of biological chemistry · 2011Article
- The two faces of Janus kinases and their respective STATs in mammary gland development and cancer.Journal of carcinogenesis · 2011Article
- Pilot study on the effects of dietary conjugated linoleic acid on tumorigenesis and gene expression in PyMT transgenic mice.Carcinogenesis · 2010Article
- Induction of the apoptosis inhibitor ARC by Ras in human cancers.The Journal of biological chemistry · 2010Article
- Nuclear factor-kappaB enhances ErbB2-induced mammary tumorigenesis and neoangiogenesis in vivo.The American journal of pathology · 2009Article
- Genetic ablation of caveolin-1 drives estrogen-hypersensitivity and the development of DCIS-like mammary lesions.The American journal of pathology · 2009Article
- Caveolin-1-/- null mammary stromal fibroblasts share characteristics with human breast cancer-associated fibroblasts.The American journal of pathology · 2009Article
- Decreased expression of caveolin 1 in patients with systemic sclerosis: crucial role in the pathogenesis of tissue fibrosis.Arthritis and rheumatism · 2008Article
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Authors and funding
7 authors.
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Abstract
During breast cancer development, the luminal space of the mammary acinar unit fills with proliferating epithelial cells that exhibit growth factor-independence, cell attachment defects, and a more invasive fibroblastic phenotype. Here, we used primary cultures of mammary epithelial cells derived from genetically engineered mice to identify caveolin-1 (Cav-1) as a critical factor for maintaining the normal architecture of the mammary acinar unit. Isolated cultures of normal mammary epithelial cells retained the capacity to generate mammary acini within extracellular matrix. However, those from Cav-1 (-/-) mice exhibited defects in three-dimensional acinar architecture, including disrupted lumen formation and epidermal growth factor-independent growth due to hyperactivation of the p42/44 mitogen-activated protein kinase cascade. In addition, Cav-1-null mammary epithelial cells deprived of exogenous extracellular matrix underwent a spontaneous epithelial-mesenchymal transition, with reorganization of the actin cytoskeleton, and E-cadherin redistribution. Mechanistically, these phenotypic changes appear to be caused by increases in matrix metalloproteinase-2/9 secretion and transforming growth factor-beta/Smad-2 hyperactivation. Finally, loss of Cav-1 potentiated the ability of growth factors (hepatocyte growth factor and basic fibroblast growth factor) to induce mammary acini branching, indicative of a more invasive fibroblastic phenotype. Thus, a Cav-1 deficiency profoundly affects mammary epithelia by modulating the activation state of important signaling cascades. Primary cultures of Cav-1-deficient mammary epithelia will provide a valuable new model to study the spatial/temporal progression of mammary cell transformation.
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