Abstract
The recently discovered p53-family member p73 displays significant homology to p53, but data from primary tumors and knockout mice argue against p73 being a classical tumor suppressor. We report on the overexpression of NH(2)-terminally truncated, transactivation-deficient p73 proteins (DeltaTA-p73) in human cancer cells. Moreover, we show that DeltaTA-p73 overexpression results in malignant transformation of NIH3T3 fibroblasts and tumor growth in nude mice, thereby providing the experimental evidence for an oncogenic function of DeltaTA-p73. Apparently, increased expression of NH(2)-terminally truncated p73 isoforms conveys the TP73 gene with oncogenic activity that appears to be actively selected for during tumor development.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3T3 Cells / metabolism
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Amino Acid Sequence
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Animals
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Carcinoma, Hepatocellular / genetics
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Carcinoma, Hepatocellular / metabolism
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Cell Transformation, Neoplastic / genetics*
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Cell Transformation, Neoplastic / metabolism
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DNA-Binding Proteins / biosynthesis
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DNA-Binding Proteins / genetics*
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Genes, Tumor Suppressor
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Humans
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Liver Neoplasms / genetics
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Liver Neoplasms / metabolism
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Mice
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Molecular Sequence Data
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Nuclear Proteins / biosynthesis
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Nuclear Proteins / genetics*
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Oncogenes / physiology*
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Protein Isoforms
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Reverse Transcriptase Polymerase Chain Reaction
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Transcriptional Activation*
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Tumor Cells, Cultured
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Tumor Protein p73
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Tumor Suppressor Proteins
Substances
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DNA-Binding Proteins
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Nuclear Proteins
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Protein Isoforms
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TP73 protein, human
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Trp73 protein, mouse
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Tumor Protein p73
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Tumor Suppressor Proteins