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ChIP-seq and RNA-seq of wildtype and NNMT-KO SUM159PT breast cancer cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE114877 | GEO | 2023/04/13

REPOSITORIES: GEO

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ChIP-seq and RNA-seq of wildtype and NNMT-KO SUM159PT breast cancer cells

Project description:ChIP-seq and RNA-seq of wildtype and NNMT-KO SUM159PT breast cancer cells

| PRJNA472961 | ENA

H3K9me3, H3K27me3, H3K27ac and H3K4me3 ChIP-sequencing in SUM159PT NNMT-WT, NNMT-KOd and NNMT KOs breast cancer cells.

Project description:The cellular heterogeneity within a tumor can be determined by core genetic and epigenetic programs that operate in certain cells (tumor initiating cells – TICs), providing them with the degree of plasticity needed for induction of metastasis and resistance to therapy. Here we show that the metabolic enzyme nicotinamide N-methyl transferase (NNMT) promotes TIC plasticity in Estrogen Receptor (ER) alpha negative breast cancer. NNMT downregulation delays tumor formation and its full depletion impairs metastasis formation in mice. Mechanistically, NNMT loss increases deposition of H3K9-me2/3 and H3K27-me3 at the promoter of genes involved in stem cell regulation, shutting down their expression and upregulating luminal differentiation genes. This study reveals a major function of NNMT in maintaining core epigenetic programmes that promote TIC self-renewal and metastasis and that repress luminal differentiation.

2023-04-13 | GSE114875 | GEO

miR205 inhibits stem cell renewal in SUM159PT breast cancer cells.

Project description:miR205 has a dual activity, as tumor suppressor and as oncogene. Here we analyzed the impact of miR205 ectopic expression in the initial tumorigenic processes of SUM159PT, a triple negative breast cancer cell line with low endogenous levels of miR205. In SUM159PT, miR205 inhibited expression of its targets VEGFA, ErbB3, Zeb1, Fyn and Lyn A/B; it reduced cell proliferation, and Myc/cyclin D1 levels, while increased p27kip1 expression. miR205 abolished anchorage-independent growth, inhibited migration and invasion, Src-kinases/Stat3 axis activation, and levels of secreted MMP9. miR205 also reduced expression of CD44 and TAZ, E2A.E12, Twist, Snail1 and CK5, associated with epithelial-mesenchymal transition (EMT). Importantly, we show that miR205 inhibited SUM159PT cancer-stem cell renewal, expression in mammospheres of CD44 and ALDH1 stem-cell markers, TAZ, and E2A.E12. All these effects of miR205 were reverted by Anti-miR205 co-expression, demonstrating its specificity. Thus, all these results strongly suggest that ectopic expression of miR205 in SUM159PT affected several parameters associated with initial steps of tumorigenesis.

| S-EPMC5705145 | biostudies-literature

H3K9me3, H3K27me3, H3K27ac and H3K4me3 ChIP-sequencing in SUM159PT NNMT-WT, NNMT-KOd and NNMT KOs breast cancer cells.

Project description:H3K9me3, H3K27me3, H3K27ac and H3K4me3 ChIP-sequencing in SUM159PT NNMT-WT, NNMT-KOd and NNMT KOs breast cancer cells.

| PRJNA472964 | ENA

SUM159PT

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-31 | GSE222596 | GEO

High-quality ChIP-seq analysis of MBD3 in human breast cancer cells.

Project description:Chromatin accessibility is tightly regulated by multiple factors/mechanisms to establish different cell type-specific gene expression programs from a single genome. Dysregulation of this process can lead to diseases including cancer. The Mi-2/nucleosome remodeling and deacetylase (NuRD) complex is thought to orchestrate chromatin structure using its intrinsic nucleosome remodeling and histone deacetylase activities. However, the detailed mechanisms by which the NuRD complex regulates chromatin structure in vivo are not yet known. To explore the regulatory mechanisms of the NuRD complex, we mapped genome-wide localization of MBD3, a structural component of NuRD, in a human breast cancer cell line (MDA-MB-231) using a modified ChIP-seq protocol. Our data showed high quality localization information (i.e., high mapping efficiency and low PCR duplication rate) and excellent consistency between biological replicates. The data are deposited in the Gene Expression Omnibus (GSE76116).

| S-EPMC4778645 | biostudies-literature

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-07-31 | E-GEOD-59937 | biostudies-arrayexpress

ChIP-seq and RNA-seq in breast cancer cell lines

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-08 | GSE195816 | GEO

ChIP-seq of HttQ111/+ and wildtype mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-05-16 | GSE150750 | GEO

Genome-wide ChIP-seq analysis of human TOP2B occupancy in MCF7 breast cancer epithelial cells.

Project description:We report the whole genome ChIP seq for human TOP2B from MCF7 cells. Using three different peak calling methods, regions of binding were identified in the presence or absence of the nuclear hormone estradiol, as TOP2B has been reported to play a role in ligand-induced transcription. TOP2B peaks were found across the whole genome, 50% of the peaks fell either within a gene or within 5?kb of a transcription start site. TOP2B peaks coincident with gene promoters were less frequently associated with epigenetic features marking active promoters in estradiol treated than in untreated cells. Significantly enriched transcription factor motifs within the DNA sequences underlying the peaks were identified. These included SP1, KLF4, TFAP2A, MYF, REST, CTCF, ESR1 and ESR2. Gene ontology analysis of genes associated with TOP2B peaks found neuronal development terms including axonogenesis and axon guidance were significantly enriched. In the absence of functional TOP2B there are errors in axon guidance in the zebrafish eye. Specific heparin sulphate structures are involved in retinal axon targeting. The glycosaminoglycan biosynthesis-heparin sulphate/heparin pathway is significantly enriched in the TOP2B gene ontology analysis, suggesting changes in this pathway in the absence of TOP2B may cause the axon guidance faults.

| S-EPMC4728365 | biostudies-literature

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