ArticleAmerican journal of respiratory cell and molecular biology2010
The loss of tuberin promotes cell invasion through the ß-catenin pathway.
Article in American journal of respiratory cell and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- CrossTORC and WNTegration in Disease: Focus on Lymphangioleiomyomatosis.International journal of molecular sciences · 2021Review
- Exploring the Role of Matrix Metalloproteinases as Biomarkers in Sporadic Lymphangioleiomyomatosis and Tuberous Sclerosis Complex. A Pilot Study.Frontiers in medicine · 2021Article
- mTOR and S6K1 drive polycystic kidney by the control of Afadin-dependent oriented cell division.Nature communications · 2020Article
- Article
- Lymphangioleiomyomatosis: a case report and review of diagnosis and treatment.OncoTargets and therapy · 2018Article
- Microbial Antigens Stimulate Metalloprotease-7 Secretion in Human B-Lymphocytes Using mTOR-Dependent and Independent Pathways.Scientific reports · 2017Article
- Lymphangioleiomyomatosis: A Monogenic Model of Malignancy.Annual review of medicine · 2017Review
- Impact of PI3K/AKT/mTOR pathway activation on the prognosis of patients with head and neck squamous cell carcinomas.Oncotarget · 2016Article
- EPIDEMIOLOGY, PATHOGENESIS and DIAGNOSIS of LYMPHANGIOLEIOMYOMATOSIS.Expert opinion on orphan drugs · 2016Article
- Article
- The RNA-binding protein Rbfox2: an essential regulator of EMT-driven alternative splicing and a mediator of cellular invasion.Oncogene · 2014Article
- Lymphangioleiomyomatosis - a wolf in sheep's clothing.The Journal of clinical investigation · 2012Review
- Tuberin regulates E-cadherin localization: implications in epithelial-mesenchymal transition.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the tumor suppressor tuberin (TSC2) are a common factor in the development of lymphangioleiomyomatosis (LAM). LAM is a cystic lung disease that is characterized by the infiltration of smooth muscle-like cells into the pulmonary parenchyma. The mechanism by which the loss of tuberin promotes the development of LAM has yet to be elucidated, although several lines of evidence suggest it is due to the metastasis of tuberin-deficient cells. Here we show that tuberin-null cells become nonadherent and invasive. These nonadherent cells express cleaved forms of β-catenin. In reporter assays, the β-catenin products are transcriptionally active and promote MMP7 expression. Invasion by the tuberin-null cells is mediated by MMP7. Examination of LAM tissues shows the expression of cleaved β-catenin products and MMP7 consistent with a model that tuberin-deficient cells acquire invasive properties through a β-catenin-dependent mechanism, which may underlie the development of LAM.
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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.