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https://www.selleckchem.com/products/trastuzumab-deruxtecan.html In recent years, sulforaphane (SFN) has been shown to have antitumor effects. To better understand the molecular basis of SFN intervention in estrogen-dependent breast cancer, integrated multi-omics data analysis was used to provide evidence and insights into molecular biology. MCF-7 breast cancer cells were treated with estradiol (E2) or/and SFN. Genome-wide DNA methylation analysis was performed by using microarray platforms. The protein profile was analyzed by TMT labeled HPLC-MS/MS. The metabolic profile was obtained by GC-MS and UPLC-MS methods. Multivariate statistics analyses, such as PCA and hierarchical clustering, were performed. The Gene Ontology (GO) and KEGG analysis were used to perform enrichment analysis of biological processes and pathways. A set of differentially methylated genes and differentially expressed proteins and metabolites were found, which indicated that SFN may reverse the adverse effects induced by E2. Integrated analysis revealed cancer genes that responded to estrogen and other pathways frequently associated with cancer. Co-pathway analysis revealed that the reversal effects of SFN were associated with purine metabolism and glutathione metabolism. The integrated omics analysis outlined a promising blueprint of the relationship of biological molecules in different dimensions, which will be beneficial for understanding the mechanism of anti-breast cancer effects and for new targets of medicines.Oxidative stress induced necroptosis is important in myocardial ischemia/reperfusion injury. Dexmedetomidine (Dex), an α2-adrenoceptor (α2-AR) agonist, has protective effect on oxidative stress induced cell apoptosis, but effects of Dex and Dex-mediated α2-AR activation on oxidant induced necroptosis was unclear. H9C2 cardiomyocytes were pre-treated with or without Dex and α2-AR antagonist yohimbine hydrochloride (YOH) before being exposed to H2O2 to induce oxidative cellular damag

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