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ΔNp73β is oncogenic in hepatocellular carcinoma by blocking apoptosis signaling via death receptors and mitochondria

p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally...

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Main Authors: Schuster, André (Author) , Schilling, Tobias (Author) , De Laurenzi, Vincenzo (Author) , Koch, Andreas Franz (Author) , Seitz, Sarah Janina (Author) , Staib, Frank (Author) , Teufel, Andreas (Author) , Thorgeirsson, Snorri S. (Author) , Galle, Peter (Author) , Melino, Gerry (Author) , Stremmel, Wolfgang (Author) , Krammer, Peter H. (Author) , Müller-Schilling, Martina (Author)
Format: Article (Journal)
Language:English
Published: 01 Jul 2010
In: Cell cycle
Year: 2010, Volume: 9, Issue: 13, Pages: 2629-2639
ISSN:1551-4005
DOI:10.4161/cc.9.13.12110
Online Access:Resolving-System, lizenzpflichtig, Volltext: https://doi.org/10.4161/cc.9.13.12110
Verlag, lizenzpflichtig, Volltext: https://www.tandfonline.com/doi/abs/10.4161/cc.9.13.12110
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Author Notes:André Schuster, Tobias Schilling, Vincenzo De Laurenzi, Andreas F. Koch, Sarah Seitz, Frank Staib, Andreas Teufel, Snorri S. Thorgeirsson, Peter Galle, Gerry Melino, Wolfgang Stremmel, Peter H. Krammer & Martina Müller
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Summary:p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis. The Trp73 gene has two promoters that drive the expression of two major p73 isoform subfamilies: TA and ΔN. In general, TAp73 isoforms show proapoptotic activities, whereas members of the N-terminally truncated (ΔN) p73 subfamily that lack the transactivation domain show antiapoptotic functions. We found that upregulation of ΔNp73 in hepatocellular carcinoma (HCC) correlated with reduced survival. Here, we investigated the molecular mechanisms accounting for the oncogenic role of ΔNp73 in HCC.
Item Description:Gesehen am 06.07.2023
Physical Description:Online Resource
ISSN:1551-4005
DOI:10.4161/cc.9.13.12110

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