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The CBF1/L3MBTL3 axis promotes the repression of Notch signaling by the histone demethylase KDM1A

ABSTRACT: We performed ChIP-seq experiments to investigate on a genome-wide scale the co-localization of CBF1 (also known as RBPJ or CSL) and L3MBTL3 on chromatin in the MDA-MB-231 cell line. Analysis of the CBF1 and L3MBTL3 ChIP-seq experiments in the MDA-MB-231 cell line revealed a substantial and significant genome-wide co-localization on chromatin, in agreement with our hypothesis that CBF1 contributes to the recruitment of L3MBTL3 to chromatin.

ORGANISM(S): Homo sapiens

PROVIDER: GSE100375 | GEO | 2017/10/12

SECONDARY ACCESSION(S): PRJNA391479

REPOSITORIES: GEO

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RBPJ/CBF1 interacts with L3MBTL3/MBT1 to promote repression of Notch signaling via histone demethylase KDM1A/LSD1

Project description:Notch signaling is an evolutionarily conserved signal transduction pathway that is essential for metazoan development. At the molecular level, the key components of the Notch pathway are the NOTCH-family receptors, the ligands of the DSL (Delta, Serrate, Lag-2) family and the transcription factor CSL [CBF1/RBPJ, Su(H), Lag-1]. Upon ligand binding, the NOTCH Intra-Cellular Domain (NOTCH ICD) translocates into the nucleus and forms a complex with RBPJ to activate the transcription of target genes. In the absence of NOTCH ICD, RBPJ acts as a transcriptional repressor. Using a proteomic approach, we identified L3MBTL3 as a novel interactor of RBPJ. We discovered that L3MBTL3 competes with NOTCH ICD for binding to RBPJ. In the absence of NOTCH ICD, RBPJ recruits L3MBTL3 and its co-factor KDM1A [lysine (K)-specific demethylase 1A] to the promoters/enhancers of Notch target genes to promote H3K4me2 demethylation and transcriptional repression. In three distinct cell contexts in which Notch signaling governs cell fate, i.e., mature T-cells as well as brain and breast tumor cells, the loss of L3MBTL3 results in the de-repression of Notch target genes. Finally, the genetic analyses of the homologs of RBPJ and L3MBTL3 in Drosophila melanogaster and Caenorhabditis elegans demonstrate that the functional link between RBPJ/Su(H)/lag-1 and L3MBTL3/dL(3)mbt/lin-61 is evolutionarily conserved, thus identifying L3MBTL3 as a universal modulator of Notch signaling in metazoans.

2017-10-17 | PXD004196 | Pride

Messenger RNA expression profiling in L3mbtl3 WT versus L3mbtl3 KO/+ mouse cerebella.

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2021-05-28 | GSE151448 | GEO

Regulatin of KDM5C stability and enhancer reprogramming in breast cancer [ChIP-Seq]

Project description:We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells. we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.

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Project description:To further investigate the molecular mechanisms by which EVs mediated the abnormal localization of tight junction proteins and adherence junction protein, we performed miRNA microarray analysis of extracellular vesicles isolated from breast cancer cells. miRNA expression in extracellular vesicles was collected from MDA-MB-231-D3H1, MDA-MB-231-D3H2LN, BMD2a and BMD2b breast cancer cell lines.

2015-04-02 | E-GEOD-63445 | biostudies-arrayexpress

Next Generation Sequencing for Chromatin accessbility by ATAC-seq for MDA-MB-231, MCF7 or HCT116 cell line

Project description:CRISPRi on PVT1 did not induce drastic changes on chromatin accessbility in MDA-MB-231 cell line. CCAT1 enhancer is accessble specifically in HCT116, not in MCF7 or MDA-MB-231.

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2020-04-28 | BIOMD0000000940 | BioModels

Gene expression profile in breast cancer cells

Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.

2019-03-19 | GSE112445 | GEO

LncRNA Uc003xsl.1 Activates of NF-κB/IL8 Axis to Promotes Triple-negative Breast Cancer Progression via A Decoy Role to NKRF [lnc231]

Project description:To discover the potential drivers of TNBC metastasis, we established an in vivo model by injecting MDA-MB-231cells into the tail veins of mice. Then, the breast tumor cells that successfully grew into metastatic lung tumors were collected and expanded in vitro, followed by re-injected into the tail veins of mice for lung metastasis. After three rounds of selection, a highly metastatic subline, MDA-MB-231-P3, was established, and more frequent micro-metastasis was detected in MDA-MB-231-P3 groups than that of MDA-MB-231 groups when the lungs of mice were stained with hematoxylin and eosin (HE). The lncRNA profiles of MDA-MB-231 or MDA-MB-231-P3 cells were analyzed by lncRNA sequencing. A total of 267 lncRNAs in MDA-MB-231-P3 cells were upregulated more than 2-fold in comparison to the MDA-MB-231 cells.

2021-11-29 | GSE163900 | GEO

DamID for MBD3 in human breast cancer cell lines [Promoter_Arrays]

Project description:Maintenance of chromatin structure is essential to eukaryotic life; dysregulation is known to be causal for aberrant development and disease. The Mi-2/nucleosome remodeling and histone deacetylase (NuRD) complex is a multiprotein machine proposed to regulate chromatin structure by nucleosome remodeling and histone deacetylation activities. We identified the localization of MBD3, a component of Mi-2/NuRD complex, in two breast cancer cell lines (MCF7 and MDA-MB-231) using ChIP-Seq. MBD3 showed cell-type specific localization with overlap across cell lines being less than 50%. MBD3 localized across gene bodies, peaking around the transcription start site (TSS). Contrary to existing models, MBD3 preferentially associated with CpG rich promoters marked by H3K4me3. These data suggest that MBD3, and by extension the Mi-2/NuRD complex, may have roles in fine tuning expression for active genes. These data represent an important first step in defining regulatory mechanisms by which Mi-2/NuRD complex controls chromatin structure and gene expression. DamID experiment was performed in human breast cancer cell lines (MCF-7 and MDA-MB-231) in duplicate. Samples were hybridized to Nimblegen 2.1M Deluxe promoter array. MBD3-Dam material was hybridized over Dam-only control.

2013-10-31 | E-GEOD-44773 | biostudies-arrayexpress

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