Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Ad-NNMT and Ad-NC Transfection on Histone Modification and Methylation in Human Umbilical Vein Endothelial Cells

ABSTRACT: This study investigates the epigenetic impact of Nicotinamide N-methyltransferase (NNMT) overexpression on human umbilical vein endothelial cells (HUVECs). HUVECs were transfected with adenovirus vectors, Ad-NC (negative control) or Ad-NNMT (overexpressing NNMT), for 48 hours. Subsequently, protein was collected for chromatin immunoprecipitation analysis using antibodies against H3K4me3 and H3K27me3 via Cut&Tag technology. To further elucidate the effects on DNA methylation, whole-genome methylation sequencing was performed. The resulting data provide insight into NNMT's regulatory role in histone modifications and methylation patterns.

ORGANISM(S): Homo sapiens

PROVIDER: GSE278939 | GEO | 2024/10/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of Ad-NNMT and Ad-NC Transfection on Histone Modification and Methylation in Human Umbilical Vein Endothelial Cells

Project description:Effect of Ad-NNMT and Ad-NC Transfection on Histone Modification and Methylation in Human Umbilical Vein Endothelial Cells

| PRJNA1169799 | 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

Proteomics reveals NNMT as a master metabolic regulator of cancer associated fibroblasts

Project description:High-grade serous carcinoma has a poor prognosis, owing primarily to its early dissemination throughout the abdominal cavity. Genomic and proteomic approaches have provided snapshots of the proteogenomics of ovarian cancer, but a systematic examination of both the tumour and stromal compartments is critical in understanding ovarian cancer metastasis. We developed a label- free proteomic workflow to analyse as few as 5,000 formalin-fixed, paraffin-embedded cells microdissected from each compartment. The tumour proteome was stable during progression from in situ lesions to metastatic disease; however, the metastasis-associated stroma was characterized by a highly conserved proteomic signature, prominently including the methyltransferase nicotinamide N-methyltransferase (NNMT) and several of the proteins that it regulates. Stromal NNMT expression was necessary and sufficient for functional aspects of the cancer-associated fibroblast (CAF) phenotype, including the expression of CAF markers and the secretion of cytokines and oncogenic extracellular matrix. Stromal NNMT expression supported ovarian cancer migration, proliferation and in vivo growth and metastasis. Expression of NNMT in CAFs led to depletion of S-adenosyl methionine and reduction in histone methylation associated with widespread gene- expression changes in the tumour stroma. This work supports the use of ultra-low-input proteomics to identify candidate drivers of disease phenotypes. NNMT is a central, metabolic regulator of CAF differentiation and cancer progression in the stroma that may be therapeutically targeted.

2019-04-18 | PXD006396 | Pride

RNA sequencing of NNMT overexpression in 3T3 fibroblasts

Project description:High grade serous carcinoma (HGSC) arising from either the fallopian tube or ovary has a poor prognosis primarily due to its early dissemination throughout the abdominal cavity. Genomic and proteomic approaches have provided snapshots of the proteogenomics of ovarian cancer (OvCa)1,2, but a systematic examination of both the tumor and stromal compartments is critical to understanding OvCa metastasis. We developed a label-free proteomic workflow to analyze as few as 5,000 formalin-fixed, paraffin embedded cells microdissected from each compartment. The tumor proteome was comparatively stable during progression from in situ lesions to metastatic disease; however, the metastasis-associated stroma was characterized by a highly conserved proteomic signature, prominently including the methyltransferase nicotinamide N-methyltransferase (NNMT) and the proteins it regulates. Stromal NNMT expression was necessary and sufficient for several functional aspects of the cancer associated fibroblast (CAF) phenotype, including the expression of CAF markers and the secretion of cytokines and oncogenic extracellular matrix. Stromal NNMT supported OvCa migration, proliferation, and in vivo growth and metastasis. Expression of NNMT in CAFs led to a depletion of S-adenosyl methionine (SAM) and a reduction in histone methylation associated with extensive gene expression changes in the tumor stroma. This work supports the use of ultra-low input proteomics to identify candidate drivers of disease phenotypes and reveals that NNMT is a central, metabolic regulator of CAF differentiation and cancer progression in the stroma and a novel treatment target.

2019-05-01 | GSE124014 | GEO

H3K27 ChIP-sequencing of NNMT overexpression in normal fibroblasts

2019-05-01 | GSE124015 | GEO

Microarray analysis of NNMT overexpression and knockdown in stromal cells

Project description:Analysis of gene expression in human CAFs with control (shCtrl) or shRNA against NNMT (shNNMT) expression or normal fibroblasts expressing control (Ctrl) or NNMT overexpression (NNMT) constructs. Cells were infected with lentivirus to express the indicated shRNA construct. Hypothesis is that knockdown of NNMT will affect expression of genes via regulation of histone methylation status.

2019-05-01 | GSE112497 | GEO

Epigenome analysis of NNMT KO versus WT cells

Project description:Genome wide methylation profiling of SUM159PT NNMT WT, KOs and KOd cells. The Illumina human Infinium Methylation EPIC BeadChip was used to measure global DNA methylation on CpG from 850 k probes. Samples include three experimental replicates from each cell line.

2023-04-24 | GSE182073 | GEO

DNA methylation analysis of NNMT overexpression and knockdown in stromal cells

Project description:Genome-wide DNA methylation profiling in response to overexpression or knockdown of NNMT in stromal cells. The Illumina MethylationEPIC array was used to profiled genome-wide methylation of normal fibroblasts expressing a control construct or NNMT overexpression construt and cancer-associated fibroblasts (CAFs) expressing an shCtrl or shNNMT construct. Two biological replicates of each experimental group were profiled following growth in 10 micromolar methionine growth media for 21 days.

2019-05-01 | GSE126672 | GEO

Microarray analysis of knockdown of nicotinamide N-methyltransferase (NNMT) in human cancer-associated fibroblasts

Project description:Analysis of gene expression in human CAFs with control (shCtrl) or shRNA against NNMT (shNNMT) expression. Cells were infected with lentivirus to express the indicated shRNA construct. Hypothesis is that knockdown of NNMT will affect expression of genes via regulation of histone methylation status.

2022-05-01 | GSE98267 | GEO

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