ArticleProceedings of the National Academy of Sciences of the United States of America1996
Suppression of tumorigenicity by the wild-type tuberous sclerosis 2 (Tsc2) gene and its C-terminal region.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 126 citations in OpenAlex.
- The role of TSC2 in breast cancer: a literature review.Frontiers in oncology · 2023Review
- Targeted therapy for mTORC1-driven tumours through HDAC inhibition by exploiting innate vulnerability of mTORC1 hyper-activation.British journal of cancer · 2020Article
- Molecular genetic diagnostics of tuberous sclerosis complex in Bulgaria: six novel mutations in theJournal of genetics · 2018Article
- VPS34 regulates TSC1/TSC2 heterodimer to mediate RheB and mTORC1/S6K1 activation and cellular transformation.Oncotarget · 2016Article
- Mesenchymal Tumorigenesis Driven by TSC2 Haploinsufficiency Requires HMGA2 and Is Independent of mTOR Pathway Activation.Cancer research · 2016Article
- Neural Crest-Specific TSC1 Deletion in Mice Leads to Sclerotic Craniofacial Bone Lesion.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015Article
- A novel androgen-regulated isoform of the TSC2 tumour suppressor gene increases cell proliferation.Oncotarget · 2014Article
- Article
- Glucose deprivation in tuberous sclerosis complex-related tumors.Cell & bioscience · 2011Article
- The loss of tuberin promotes cell invasion through the ß-catenin pathway.American journal of respiratory cell and molecular biology · 2010Article
- Tuberin regulates E-cadherin localization: implications in epithelial-mesenchymal transition.The American journal of pathology · 2010Article
- Quantitative mass spectrometry of diabetic kidney tubules identifies GRAP as a novel regulator of TGF-beta signaling.Biochimica et biophysica acta · 2010Article
- Rheb controls misfolded protein metabolism by inhibiting aggresome formation and autophagy.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- A GSK-3/TSC2/mTOR pathway regulates glucose uptake and GLUT1 glucose transporter expression.American journal of physiology. Cell physiology · 2008Article
- In silico regulatory analysis for exploring human disease progression.Biology direct · 2008Article
- Phospholipase D1 is an effector of Rheb in the mTOR pathway.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- The TSC1-TSC2 complex: a molecular switchboard controlling cell growth.The Biochemical journal · 2008Review
- Abnormal growth of smooth muscle-like cells in lymphangioleiomyomatosis: Role for tumor suppressor TSC2.American journal of respiratory cell and molecular biology · 2006Article
- Rap1GAP inhibits tumor growth in oropharyngeal squamous cell carcinoma.The American journal of pathology · 2006Article
- Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling.Genes & development · 2003Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Tsc2 gene, which is mutationally inactivated in the germ line of some families with tuberous sclerosis, encodes a large, membrane-associated GTPase activating protein (GAP) designated tuberin. Studies of the Eker rat model of hereditary cancer strongly support the role of Tsc2 as a tumor suppressor gene. In this study, the biological activity of tuberin was assessed by expressing the wild-type Tsc2 gene in tumor cell lines lacking functional tuberin and also in rat fibroblasts with normal levels of endogenous tuberin. The colony forming efficiency of Eker rat-derived renal carcinoma cells was significantly reduced following reintroduction of wild-type Tsc2. Tumor cells expressing the transfected Tsc2 gene became more anchorage-dependent and lost their ability to form tumors in severe combined immunodeficient mice. At the cellular level, restoration of tuberin expression caused morphological changes characterized by enlargement of the cells and increased contact inhibition. As with the full-length Tsc2 gene, a clone encoding only the C terminus of tuberin (amino acids 1049-1809, including the GAP domain) was capable of reducing both colony formation and in vivo tumorigenicity when transfected into the Eker rat tumor cells. In normal Rat1 fibroblasts, conditional overexpression of tuberin also suppressed colony formation and cell growth in vitro. These results provide direct experimental evidence for the tumor suppressor function of Tsc2 and suggest that the tuberin C terminus plays an important role in this activity.
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