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• W2078214009 endingPage "4578" @default.
• W2078214009 startingPage "4565" @default.
• W2078214009 abstract "Inactivating mutations within the von Hippel-Lindau (VHL) tumor suppressor gene predispose patients to develop a variety of highly vascularized tumors. pVHL targets α subunits of the heterodimeric transcription factor hypoxia-inducible factor (HIF), a critical regulator of energy metabolism, angiogenesis, hematopoiesis, and oxygen (O2) delivery, for ubiquitin-mediated degradation in an O2-dependent manner. To investigate the role of Vhl in cellular proliferation and tumorigenesis, we utilized mouse embryonic fibroblasts (MEFs), a common tool for analyzing cell cycle regulation, and generated Vhl−/− MEF-derived fibrosarcomas. Surprisingly, growth of both Vhl−/− MEFs and fibrosarcomas was impaired, although tumor vascularity was increased. Decreased proliferation of Vhl−/− MEFs was correlated with an overexpression of cyclin kinase inhibitors (CKIs) p21 and p27. The transcription of p21 and p27 is inhibited by c-Myc; therefore, the induction of CKIs was attributed to the ability of HIF to antagonize c-Myc activity. Indeed, p21 mRNA levels were elevated under normoxia in Vhl−/− MEFs, while c-Myc transcriptional activity was markedly reduced. Gene silencing of HIF-1α by small interfering RNA reduced p21 and p27 protein and mRNA levels in Vhl−/− MEFs. The induction of p21 and p27, mediated by constitutive activation of the HIF pathway, provides a mechanism for the decreased proliferation rates of Vhl−/− MEFs and fibrosarcomas. These results demonstrate that a loss of pVHL can induce growth arrest in certain cells types, which suggests that additional genetic mutations are necessary for VHL-associated tumorigenesis." @default.
• W2078214009 created "2016-06-24" @default.
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• W2078214009 date "2005-06-01" @default.
• W2078214009 modified "2023-09-26" @default.
• W2078214009 title "Decreased Growth of <i>Vhl</i>^{−<i>/</i>−} Fibrosarcomas Is Associated with Elevated Levels of Cyclin Kinase Inhibitors p21 and p27" @default.
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• W2078214009 doi "https://doi.org/10.1128/mcb.25.11.4565-4578.2005" @default.
• W2078214009 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1140627" @default.
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