ArticleGenome research2023
Loss of epigenetic suppression of retrotransposons with oncogenic potential in aging mammary luminal epithelial cells.
Article in Genome research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
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- The breakome of BRCA1 and BRCA2 pathway mutation carriers reveals early processes in breast oncogenesis.Cell death & disease · 2025Article
- Overexpression of SOX4 in MSCs inhibits cellular senescence and enhances therapeutic efficacy in systemic lupus erythematosus.Stem cell research & therapy · 2025Article
- Exploring the Relationship of Transposable Elements and Ageing: Causes and Consequences.Genome biology and evolution · 2025Review
- Transposon activity and nucleotide triplet instability: new perspectives on their potential interplay in brain disorders.Frontiers in neuroscience · 2025Article
- Marker genes reveal dynamic features of cell evolving processes.Bioinformatics advances · 2025Article
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- Epigenetic clocks and programmatic aging.Ageing research reviews · 2024Review
- IRescue: uncertainty-aware quantification of transposable elements expression at single cell level.Nucleic acids research · 2024Article
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- Methylation entropy landscape of Chinese long-lived individuals reveals lower epigenetic noise related to human healthy aging.Aging cell · 2024Article
- A critical review of the recent concept of regulatory performance of DNA Methylations, and DNA methyltransferase enzymes alongside the induction of immune microenvironment elements in recurrent pregnancy loss.Toxicology reports · 2024Review
- Epigenomic insights into common human disease pathology.Cellular and molecular life sciences : CMLS · 2024Review
- Review
- Comprehensive single cell aging atlas of mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
A primary function of DNA methylation in mammalian genomes is to repress transposable elements (TEs). The widespread methylation loss that is commonly observed in cancer cells results in the loss of epigenetic repression of TEs. The aging process is similarly characterized by changes to the methylome. However, the impact of these epigenomic alterations on TE silencing and the functional consequences of this have remained unclear. To assess the epigenetic regulation of TEs in aging, we profiled DNA methylation in human mammary luminal epithelial cells (LEps)-a key cell lineage implicated in age-related breast cancers-from younger and older women. We report here that several TE subfamilies function as regulatory elements in normal LEps, and a subset of these display consistent methylation changes with age. Methylation changes at these TEs occurred at lineage-specific transcription factor binding sites, consistent with loss of lineage specificity. Whereas TEs mainly showed methylation loss, CpG islands (CGIs) that are targets of the Polycomb repressive complex 2 (PRC2) show a gain of methylation in aging cells. Many TEs with methylation loss in aging LEps have evidence of regulatory activity in breast cancer samples. We furthermore show that methylation changes at TEs impact the regulation of genes associated with luminal breast cancers. These results indicate that aging leads to DNA methylation changes at TEs that undermine the maintenance of lineage specificity, potentially increasing susceptibility to breast cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.