Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1169547 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30895883_1.fastq.gz | Fastqsanger.gz | |||
| SRR30895883_2.fastq.gz | Fastqsanger.gz | |||
| SRR30895884_1.fastq.gz | Fastqsanger.gz | |||
| SRR30895884_2.fastq.gz | Fastqsanger.gz |
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Project description:Catechol estrogens (CEs) are metabolic electrophiles that actively undergo covalent interaction with cellular proteins, influencing molecular function. There is no feasible method to identify their binders in a living system. Herein, we developed a click chemistry-based approach using ethinylestradiol(EE2) as the precursor probe coupled with quantitative proteomics to identify protein targets of CEs and classify their binding strengths.
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Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer (BC) cells. To delineate COMT role in metastasis of estrogen receptor (ER) dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A BC model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). We performed comparative gene expression analysis using data obtained from RNA-seq of COMT-overexpressing and control cells in biological duplicates.
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Project description:Catechol estrogens (CEs) are known to be toxic metabolites and the initiators in the oncogenesis of breast cancers via forming covalent adducts with DNAs. CEs shall also react with proteins but their cellular protein targets remain un-explored. Here we reported the identification of protein targets of CEs in the soluble cytosol of estrogen-sensitive breast cancer cells by multiple comparative proteomics using liquid chromatography tandem mass spectrometry (LC-MS/MS) coupled with an improved click chemistry-based workflow. Multiple comparative proteomics composed of experimental pair (probe versus solvent) and two control pairs (solvent versus solvent and probe versus solvent without enrichment), were studied using stable isotope dimethyl labeling. The use of 4-hydroxyethynylestradiol (4OHEE2) probe with an amide-free linker coupled with on-bead digestion and re-digestion of the proteins cleaved from the beads was shown to greatly improve the recovery and identification of CEs-adducted peptides. A total of 310 protein targets and 35 adduction sites were repeatedly (n≥2) identified with D/H (probe/solvent) ratio >4 versus only one identified with D/H >4 from the two control pairs, suggesting that our workflow imposes only a very low background. Meanwhile, multiple comparative D/H ratios revealed that CEs may down-regulate many target proteins involved in the metabolism or detoxification, suggesting a negative correlation between CEs-induced adduction and expression of proteins acting on the alleviation of stress-induced cellular damages. The reported method and data shall provide opportunities to study the progression of estrogen metabolism-derived diseases and biomarkers.
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Project description:The goal of this study is to obtain a genomic view of the Fur regulatory network under both iron replete and iron deficient conditions in Bacillus subtilis using ChIP-seq. Besides the known Fur target sites, 70 putative DNA binding sites were identified, and the vast majority had higher occupancy under iron sufficient conditions. In addition,we discovered a role for catechol degradation in bacillibactin metabolism, and provided evidence that catechol 2,3-dioxygenase can detoxify endogenously produced catechol substrates in addition to its more widely studied role in biodegradation of environmental aromatic compounds and pollutants.
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Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer cells. To delineate COMT role in metastasis of estrogen receptor dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating COMT overexpression in MCF7 breast cancer cell line, and results of pulldown analysis of COMT-interacting proteins in MCF7 cells.
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