Loss of PTEN facilitates HIF-1-mediated gene expression
Open accessAbstract
In glioblastoma-derived cell lines, PTEN does not significantly alter apoptotic sensitivity or cause complete inhibition of DNA synthesis. However, in these cell lines PTEN regulates hypoxia- and IGF-1-induced angiogenic gene expression by regulating Akt activation of HIF-1 activity. Restoration of wild-type PTEN to glioblastoma cell lines lacking functional PTEN ablates hypoxia and IGF-1 induction of HIF-1-regulated genes. In addition, Akt activation leads to HIF-1alpha stabilization, whereas PTEN attenuates hypoxia-mediated HIF-1alpha stabilization. We propose that loss of PTEN during malignant progression contributes to tumor expansion through the deregulation of Akt activity and HIF-1-regulated gene expression.
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Inactivating mutations in PTEN or TSC, as well as activating mutations in PI3K or AKT, lead to increased TORC1 activity that promotes HIF-α stabilization.
“Inactivating mutations in phosphatase and tensin homolog (PTEN) or the tuberosis sclerosis complex (TSC) complex, as well as activating mutations in phosphatidylinositol 3-kinase (PI3K) or AKT, lead to increased TORC1 activity that promotes HIF-α stabilization”
From Hypoxic control of metastasis (2016) · cites this paper as [31]
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References 40 · Cited by 840
- Authors
- Zundel, W., Schindler, C., Haas-Kogan, D., Koong, A., Kaper, F., Chen, E., Gottschalk, A. R., Ryan, H. E., Johnson, R. S., Jefferson, A. B., Stokoe, D., & Giaccia, A. J.
- Affiliations
- University of California, San Francisco (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2000-02-15
- Volume
- 14
- Issue
- 4
- Pages
- 391-396
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC316386
- OpenAlex
- W2129873928
- Cited by
- 840
- References
- 40
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 13 · 2023: 13 · 2022: 9 · 2021: 14 · 2020: 13 · 2019: 20 · 2018: 10 · 2017: 23 · 2016: 24 · 2015: 27 · 2014: 35 · 2013: 38 · 2012: 33
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Radiological Society of North America
- National Institutes of Health (5r01ca073832-02, CA67166)
- National Cancer Institute (P01CA067166, CA09302, CA 67166, CA 73832, T32CA009302)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Keywords
- PTEN, HIF-1, glioblastoma, Akt signaling, HIF-1α stabilization, hypoxia, insulin-like growth factor I, angiogenesis, tumor angiogenesis, tumor progression, tumor suppressor loss
- MeSH terms
- Brain Neoplasms, DNA-Binding Proteins, Genetic Complementation Test, Glioblastoma, Humans, Insulin-Like Growth Factor I, Isoenzymes, Lymphokines, Membrane Proteins, Neoplasm Proteins, Nuclear Proteins, Phosphofructokinase-1, Phosphoric Monoester Hydrolases, Prostaglandin-Endoperoxide Synthases, Proto-Oncogene Proteins, Recombinant Fusion Proteins, Transcription Factors, Transfection, Tumor Cells, Cultured, Cell Hypoxia, Gene Expression Regulation, Neoplastic, Endothelial Growth Factors, Culture Media, Serum-Free, Apoptosis, Protein Serine-Threonine Kinases, Gene Deletion, Phosphotransferases (Alcohol Group Acceptor), Disease Progression, Tumor Suppressor Proteins, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Proto-Oncogene Proteins c-akt, PTEN Phosphohydrolase, Cyclooxygenase 1, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit
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