Abstract
We have recently reported a connection between the expression of the Werner syndrome gene (WRN), whose loss of function has been implicated in a human progeroid syndrome (WS), and the Myc oncoprotein. Myc overexpression directly elevates trancription of the WRN gene, whose presence is required to avoid senescence during Myc proliferative stimuli. Here we discuss several hypotheses to explain why WRN might be required to support oncogenic proliferation in light of the known function of WRNprotein and Myc in genomic instability and transcriptional modulation. In addition, we address the apparent paradox of why patients with WS, lacking WRN function, have increased incidence of certain cancers.
MeSH terms
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Animals
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Cell Division / physiology
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Cell Transformation, Neoplastic / genetics*
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Cellular Senescence / genetics
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Cellular Senescence / physiology*
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DNA Helicases / genetics
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DNA Helicases / metabolism*
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DNA-Binding Proteins
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Exodeoxyribonucleases
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Genes, myc / genetics
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Genes, myc / physiology*
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Humans
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Lymphoma / complications
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Lymphoma / genetics
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Mutation
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Promoter Regions, Genetic / genetics
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RNA, Small Interfering / metabolism
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RecQ Helicases
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Telomerase / metabolism
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Tumor Cells, Cultured
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Werner Syndrome / complications
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Werner Syndrome / genetics*
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Werner Syndrome Helicase
Substances
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DNA-Binding Proteins
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RNA, Small Interfering
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Telomerase
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Exodeoxyribonucleases
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DNA Helicases
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RecQ Helicases
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WRN protein, human
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Werner Syndrome Helicase