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H3K27 ChIP-sequencing of NNMT overexpression in normal fibroblasts

ABSTRACT: H3K27 ChIP-sequencing of NNMT overexpression in normal fibroblasts

PROVIDER: PRJNA510590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8345990.fastq.gz	Fastqsanger.gz
	SRR8346000.fastq.gz	Fastqsanger.gz
	SRR8345991.fastq.gz	Fastqsanger.gz
	SRR8346001.fastq.gz	Fastqsanger.gz
	SRR8345992.fastq.gz	Fastqsanger.gz

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H3K27 ChIP-sequencing of NNMT overexpression in normal 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.

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Overexpression of circCUL2 in normal fibroblasts

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RNA sequencing of NNMT overexpression in 3T3 fibroblasts

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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

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

Overexpression of circCUL2 in normal fibroblasts

Project description:We have found through previous experiments that circCUL2 acts as a key regulator of cancer-associated fibroblasts activation. To determine how circCUL2 exert its function, we performed mRNA sequencing of normal fibroblasts (NFs) and circCUL2-transduced NFs. 48 hours after transfection, RNA was isolated and sent for total RNA sequencing. Differential gene expression between circCUL2-overexpression and empty vector revealed enrichment for several inflammation pathways implicating involvement of these pathways in inflammatory cancer-associated fibroblasts activation.

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Fibroblasts: Normal fibroblasts vs. Carcinoma-associated fibroblasts

Project description:Transcriptional profiling of human carcinoma-associated fibroblasts (CAFs) comparing control normal fibroblasts (NFs). NFs derived from normal tissues and CAFs derived from the patients with oral cancer were identified by immunocytochemistry. Goal was to determine differentially expressed lncRNAs between NFs and CAFs.

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RNA sequencing of NNMT overexpression in 3T3 fibroblasts

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Gene expression data from normal human atrial cardiac fibroblasts, normal human ventricular cardiac fibroblasts, normal human dermal fibroblasts, human bone marrow-derived mesenchymal stem cells and human iPS cell-derived fibroblasts.

Project description:Comparison of gene expression profiles in three samples of normal human atrial cardiac fibroblasts, normal human ventricular cardiac fibroblasts, normal human dermal fibroblasts, human bone marrow-derived mesenchymal stem cells and human iPS cell-derived fibroblasts using microarray analysis.

2023-03-20 | GSE202991 | GEO

Differentially expressed genes affected by CSRNP1 overexpression in human-derived vaginal fibroblasts

Project description:Pelvic organ prolapse (POP) is a group of diseases caused by extracellular matrix (ECM) degradation in the pelvic supportive tissues. Cysteine and serine rich nuclear protein 1 (CSRNP1) is involved in cell proliferation and survival regulation, and reportedly facilitates collagen breakdown in human chondrocytes. We here uncovered CSRNP1 as a key driver on collagen degradation in human-derived vaginal fibroblasts. Apoptosis of POP patient-derived vaginal fibroblasts was suppressed after knocking down CSRNP1. Silencing of CSRNP1 inhibited hydrogen peroxide (H2O2)-triggered apoptosis, ROS generation and collagen loss in normal vaginal fibroblasts. In line with this, CSRNP1 overexpression led to proliferation inhibition, apoptosis and collagen degradation in normal subject-derived vaginal fibroblasts. Silencing of CSRNP1 also reduced the expression of cell senescence markers p21 and γ-H2Ax (the histone H2Ax phosphorylated at Ser139), as well as curbed collagen breakdown in normal vaginal fibroblasts caused by a DNA damage agent etoposide. Transcriptomic analysis showed that differentially expressed genes affected by CSRNP1 overexpression in normal vaginal fibroblasts were mainly enriched in the Wnt signaling pathway, which was crucial for the onset and progression of POP. Silencing of CSRNP1 upregulated the expression of nuclear β-catenin and induced nuclear translocation of β-catenin in H2O2-induced normal vaginal fibroblast. Furthermore, collagen deposition caused by CSRNP1 knockdown was curbed after treatment with a Wnt pathway inhibitor DKK1. Our study indicates that the CSRNP1 may be involved in POP progression through the Wnt signaling, which provides a potential therapeutic strategy for POP.

2024-05-27 | GSE268081 | GEO

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