{"title":"Epigenetic dysregulation of retrotransposons in cancer.","authors":"Danny Leung, Kwok Yu Liu","doi":"10.1158/1541-7786.MCR-24-0744","DOIUrl":null,"url":null,"abstract":"<p><p>Approximately 97% of the human genome comprises non-coding sequences, with nearly half originating from transposable elements. Among these, retrotransposons represent a critical subclass that replicates via a \"copy-and-paste\" mechanism and significantly influences the regulation of host genomes. In both normal and pathological contexts, retrotransposons contribute a vast reservoir of regulatory elements that can modulate the expression of genes. If left unchecked, retrotransposons can substantially affect host transcriptional programs and genomic integrity. Therefore, various mechanisms, including epigenetic modifications, are employed to mitigate their potentially deleterious effects. In diseases such as cancers, the epigenome is often significantly reprogrammed, which can lead to retrotransposon dysregulation. Drawing insights from recent studies conducted in human and murine cells, this review examines how retrotransposons expand the complexity of mammalian genomes, describes the impact of their epigenetic dysregulation in cancer development, and highlights the potential of targeting these sequences for therapeutic strategies.</p>","PeriodicalId":19095,"journal":{"name":"Molecular Cancer Research","volume":" ","pages":""},"PeriodicalIF":4.1000,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Cancer Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1158/1541-7786.MCR-24-0744","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Approximately 97% of the human genome comprises non-coding sequences, with nearly half originating from transposable elements. Among these, retrotransposons represent a critical subclass that replicates via a "copy-and-paste" mechanism and significantly influences the regulation of host genomes. In both normal and pathological contexts, retrotransposons contribute a vast reservoir of regulatory elements that can modulate the expression of genes. If left unchecked, retrotransposons can substantially affect host transcriptional programs and genomic integrity. Therefore, various mechanisms, including epigenetic modifications, are employed to mitigate their potentially deleterious effects. In diseases such as cancers, the epigenome is often significantly reprogrammed, which can lead to retrotransposon dysregulation. Drawing insights from recent studies conducted in human and murine cells, this review examines how retrotransposons expand the complexity of mammalian genomes, describes the impact of their epigenetic dysregulation in cancer development, and highlights the potential of targeting these sequences for therapeutic strategies.
期刊介绍：
Molecular Cancer Research publishes articles describing novel basic cancer research discoveries of broad interest to the field. Studies must be of demonstrated significance, and the journal prioritizes analyses performed at the molecular and cellular level that reveal novel mechanistic insight into pathways and processes linked to cancer risk, development, and/or progression. Areas of emphasis include all cancer-associated pathways (including cell-cycle regulation; cell death; chromatin regulation; DNA damage and repair; gene and RNA regulation; genomics; oncogenes and tumor suppressors; signal transduction; and tumor microenvironment), in addition to studies describing new molecular mechanisms and interactions that support cancer phenotypes. For full consideration, primary research submissions must provide significant novel insight into existing pathway functions or address new hypotheses associated with cancer-relevant biologic questions.
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