Abstract
Approximately 45% of the human genome is composed of transposable elements (TEs). Expression of these elements is tightly regulated during normal development. TEs may be expressed at high levels in embryonic stem cells but are epigenetically silenced in terminally differentiated cells. As part of the global 'epigenetic dysregulation' that cells undergo during transformation from normal to cancer, TEs can lose epigenetic silencing and become transcribed, and, in some cases, active. Here, we summarize recent advances detailing the consequences of TE activation in cancer and describe how these understudied residents of our genome can both aid tumorigenesis and potentially be harnessed for anticancer therapies.
Keywords:
ERVs; LINE-1; LINEs; P53; SINEs; cancer; epigenetics; transposable elements; viral mimicry.
© 2021 Federation of European Biochemical Societies.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antineoplastic Agents / therapeutic use
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Carcinogenesis / genetics
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Carcinogenesis / metabolism
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Carcinogenesis / pathology
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Cell Differentiation
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DNA Methylation*
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DNA Transposable Elements*
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Epigenesis, Genetic*
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Gene Expression Regulation, Neoplastic*
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Gene Silencing
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Human Embryonic Stem Cells / metabolism
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Human Embryonic Stem Cells / pathology
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Humans
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Long Interspersed Nucleotide Elements
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Metabolic Networks and Pathways / drug effects
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Metabolic Networks and Pathways / genetics*
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Mutagenesis, Insertional
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Neoplasms / drug therapy
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Neoplasms / genetics*
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Neoplasms / metabolism
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Neoplasms / pathology
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Protein Processing, Post-Translational
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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Antineoplastic Agents
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DNA Transposable Elements
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Tumor Suppressor Protein p53