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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

Project description:Genome wide DNA methylation profiling of luminal epithelial cells obtained from reduction mammoplasty tissue from younger (<30 year) and older (>55 year) individuals.

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Proteomic and phosphoproteomic profiling of aging human mammary myoepithelial and luminal epithelial cells

Project description:The aim of this project is to examine age-dependent changes in the proteomes and phosphoproteomes of normal human mammary luminal epithelial and myoepithelial cells.

2021-11-03 | PXD027540 | Pride

LSD1 maintains mammary luminal cell differentiation and suppresses luminal breast cancer cell invasion

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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GATA3 Reprograms Basal Breast Cancer Cells towards a Luminal Subtype and Inhibits Metastases through Suppression of Lysyl Oxidase

Project description:The transcription factor GATA3 is essential for luminal cell differentiation during mammary gland development and critical for formation of the luminal subtypes of breast cancer. Ectopic expression of GATA3 promoted global alterations of the transcriptome of basal triple-negative breast cancer cells resulting in molecular and cellular changes associated with a more differentiated, luminal tumor subtype and a concomitant reduction in primary tumor growth, lung metastasis, and macrophage recruitment at the metastatic site. Importantly, we demonstrate that the inhibition of metastases by GATA3 results from the suppression of lysyl oxidase (LOX) expression, a metastasis promoting matrix protein that affects cell proliferation, cross-linking of extracellular collagen types, and establishment of the metastatic niche. There are 2 samples sent in triplicates.

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Transcription profiling of human lung epithelial cells ollowing oncogenic KRAS expression and TBK1 suppression or infection with oncogenic KRAS (G12V) - SuperSeries

Project description:The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. An alternative strategy for targeting KRAS is to identify gene products that, when suppressed or inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference (RNAi) to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkB kinase, TBK1, was selectively essential in cells that harbor mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF- B anti-apoptotic signals involving cREL and BCL-XL that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations identify TBK1 as a potential therapeutic target in KRAS mutant tumors and establish a general approach for the rational identification of co-dependent pathways in cancer. This SuperSeries is composed of the following subset Series:; GSE17643: Profiling of immortalized human lung epithelial cells following oncogenic KRAS expression and TBK1 suppression; GSE17671: Profiling of immortalized human lung epithelial cells following infection with oncogenic KRAS (G12V) Experiment Overall Design: Refer to individual Series

2009-10-31 | E-GEOD-17672 | biostudies-arrayexpress

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Project description:The mammary epithelia are mainly composed of two distinct lineages, the basal and luminal cells. In our MMTV-Cre; Brca1flox/flox mouse model, we found the Brca1 knockout mainly occurred in the luminal cells, which will lead the mammary tumorigenesis. To investigate the Brca1 deficiency mediated mammary tumorigenesis, we sorted the luminal cells from wild type mice and MMTV-Cre; Brca1flox/flox mice for RNAseq analysis.

2021-11-17 | GSE148613 | GEO

Direct cell-to-cell transmission of retrotransposons

Project description:Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of LTR retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, with structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions, enabling the direct transfer of retrotransposon capsids into the oocyte. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses, offering important insights into host-pathogen evolution and soma-germline interactions.

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JNK2 inhibits mammary luminal cell commitment

Project description:JNK2 inhibits mammary luminal cell commitment

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Expression data from freshly isolated mouse mammary luminal cells

Project description:The mammary luminal cell compartment is heterogeneous. In adult virgin mice, it contains clonogenic luminal progenitors and non-clonogenic luminal cells expressing estrogen and progesterone receptors that can be discrimated by their cell surface expression of ICAM-1. We have separated ICAM1+ luminal progenitors and ICAM- non-clonogenic luminal cells and analyzed their transcriptomic profiles. After showing that the luminal progenitor population overexpressed Met, Trp53 and numerous p53 target genes, we analyzed how the p53 and Met signaling pathways cooperate to control the function and plasticity of luminal progenitors.

2019-02-05 | GSE122928 | GEO

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