Abstract
Telomere maintenance is essential for cellular immortality, and most cancer cells maintain their telomeres through the enzyme telomerase. Telomeres and telomerase represent promising anticancer targets. However, 15% of cancer cells maintain their telomeres through alternative recombination-based mechanisms, and previous analyses showed that recombination-based telomere maintenance can be activated after telomerase inhibition. We determined whether telomeric recombination can also be promoted by telomere dysfunction. We report for the first time that telomeric recombination can be induced in human telomerase-positive cancer cells with dysfunctional telomeres.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Ataxia Telangiectasia Mutated Proteins
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Breast Neoplasms
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Cell Cycle Proteins / metabolism
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Cell Line, Tumor
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DNA, Circular / biosynthesis
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DNA-Binding Proteins / metabolism
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Female
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Humans
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In Situ Hybridization, Fluorescence
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Intracellular Signaling Peptides and Proteins / metabolism
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Mutation
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Protein Serine-Threonine Kinases / metabolism
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Recombination, Genetic*
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Sister Chromatid Exchange
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Telomerase / biosynthesis*
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Telomerase / genetics
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Telomere / genetics
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Telomere / metabolism*
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Telomeric Repeat Binding Protein 1 / metabolism
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Tumor Suppressor Proteins / metabolism
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Tumor Suppressor p53-Binding Protein 1
Substances
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Cell Cycle Proteins
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DNA, Circular
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DNA-Binding Proteins
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Intracellular Signaling Peptides and Proteins
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TP53BP1 protein, human
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Telomeric Repeat Binding Protein 1
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Tumor Suppressor Proteins
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Tumor Suppressor p53-Binding Protein 1
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ATM protein, human
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Ataxia Telangiectasia Mutated Proteins
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Protein Serine-Threonine Kinases
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Telomerase