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Loss of epigenetic suppression of retrotransposons with oncogenic potential in aging mammary luminal epithelial cells

ABSTRACT: Loss of epigenetic suppression of retrotransposons with oncogenic potential in aging mammary luminal epithelial cells

PROVIDER: PRJNA642137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12095888_1.fastq.gz	Fastqsanger.gz
	SRR12095888_2.fastq.gz	Fastqsanger.gz
	SRR12095889_1.fastq.gz	Fastqsanger.gz
	SRR12095889_2.fastq.gz	Fastqsanger.gz
	SRR12095890_1.fastq.gz	Fastqsanger.gz

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Loss of epigenetic suppression of retrotransposons with oncogenic potential in aging mammary luminal epithelial cells.

Project description: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.

| S-EPMC10547379 | biostudies-literature

Loss of epigenetic suppression of retrotransposons with oncogenic potential in aging mammary luminal epithelial cells

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Project description:LSD1 (KDM1A) is a histone demethylase that plays both oncogenic and tumor suppressor roles in breast cancer. However, the exact contexts under which it plays these opposite roles remain largely elusive. By characterizing its role in normal and cancerous luminal mammary epithelial cells (MECs), here we show that LSD1 is essential for maintaining differentiation and survival of luminal cells. LSD1-inhibition by both genetic and pharmacological approaches increases invasion of luminal breast cancer cells. Mechanistically, we find LSD1 interacts with GATA3 and their common target genes are highly related to breast cancer. LSD1 positively regulates GATA3 expression and represses that of TRIM37, a histone H2A ubiquitin ligase and breast cancer oncoprotein. LSD1-loss leads to reduced expression of several cell junction genes (e.g., CDH1, VCL, CTNNA1), possibly via TRIM37-mediated repression. Collectively, our data suggest LSD1 largely plays a tumor suppressor role in luminal breast cancer and the increased MEC invasiveness associated with LSD1-inhibition can be blocked via TRIM37-inhibition.

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