Dataset Information

N-glycopeptide Signatures in Liver Diseases

ABSTRACT: (1) A N-glycopeptide method based on 18O/16O C-terminal labelling to obtain comparisons of serum from patients with HBV-related hepatocellular carcinoma (HCC-O18 labelling) and HBV-related liver cirrhosis (LC-O16 labelling) (2) MRM verification of N-glycopeptide alterations

ORGANISM(S): Homo Sapiens

SUBMITTER: Haojie Lu

PROVIDER: PXD013586 | iProX | Tue Sep 10 00:00:00 BST 2019

REPOSITORIES: iProX

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Publications

N-glycopeptide Signatures of IgA<sub>2</sub> in Serum from Patients with Hepatitis B Virus-related Liver Diseases.

Zhang Shu S Cao Xinyi X Liu Chao C Li Wei W Zeng Wenfeng W Li Baiwen B Chi Hao H Liu Mingqi M Qin Xue X Tang Lingyi L Yan Guoquan G Ge Zefan Z Liu Yinkun Y Gao Qiang Q Lu Haojie H

Molecular & cellular proteomics : MCP 20190909 11

N-glycosylation alteration has been reported in liver diseases. Characterizing N-glycopeptides that correspond to N-glycan structure with specific site information enables better understanding of the molecular pathogenesis of liver damage and cancer. Here, unbiased quantification of N-glycopeptides of a cluster of serum glycoproteins with 40-55 kDa molecular weight (40-kDa band) was investigated in hepatitis B virus (HBV)-related liver diseases. We used an N-glycopeptide method based on <sup>18< ...[more]

PMID: 31501225

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Project description:Purpose: Aberrantly methylated DNA are hallmarks for many cancers, HCC included. Tumor shed its DNA into circulation stream, and serum DNA methylation analysis is a less-invasive and accessable way to judge the primary tumor status. The goals of this study are to compare DNA methylation profiling in serum cell-free DNA from different stages of HCC progression including healthy control, chronic HBV carrier, HBV-related liver Cirrhosis and HCC, to establish HCC development-related aberrnat DNA methylation patterns. Methods: MBD methylCap/seq was carried out to screen differentially methylated CpG islands in serum cell-free DNA on four different stage of HBV-related HCC development. MSP and multiplex-BSP validation was performed using independent serum DNA or tumor and adjacent tissues. Results: Using a MBD methylCap/seq platform, we produced 33- to 37- million raw reads per sample and mapped them, in about half of the raw reads, to human genome(build h19) in the serum cf DNA of healthy control, HBV carrier, HBV cirrhosis and HCC. The mapped reads formed 180k to 260k peaks per sample, with 160 k common peaks shared by four samples. After subtraction of the common peaks, there left 51k, 107k and 78 k DMRs representing hypermethylations, in HBV carrier, HBV cirrhosis and HCC, respectively. We define those DMRs as early, middle and late when these DMRS occurred and maintained in HBV carrier, HBV cirrhosis and HCC, which including 27k, 24k and 19k DMRs, corresponding to 1,416, 1,337, 1,006 genes. GO analysis of them revealed gene categories and pathways associated with tumorogenenisis related process Conclusions: Our study represents the first detailed analysis of serum cf-DNA methylation profiling in the progression of HBV related HCC development. The processed data analysis here offers a comprehensive evaluation of DNA methylation in serum cf DNA. We conclude that MBD methylCap/seq based methylation profiling would benefit epigenetic research in HCC.

Project description:To unravel molecular targets involved in glycopeptide resistance, three isogenic strains of Staphylococcus aureus with different susceptibility levels to vancomycin or teicoplanin were subjected to whole-genome microarray-based transcription and quantitative proteomic profiling. Quantitative proteomics performed on membrane extracts showed exquisite inter-experimental reproducibility permitting the identification and relative quantification of >30% of the predicted S. aureus proteome. In the absence of antibiotic selection pressure, comparison of stable resistant and susceptible strains revealed 94 differentially expressed genes and 178 proteins. As expected, only partial correlation was obtained between transcriptomic and proteomic results during stationary-phase. Application of massively parallel methods identified one third of the complete proteome, a majority of which was only predicted based on genome sequencing, but never identified to date. Several over‑expressed genes represent previously reported targets, while series of genes and proteins possibly involved in the glycopeptide resistance mechanism were discovered here, including regulators, global regulator attenuator, hyper‑mutability factor or hypothetical proteins. Gene expression of these markers was confirmed in a collection of genetically unrelated strains showing altered susceptibility to glycopeptides. Our proteome and transcriptome analyses have been performed during stationary‑phase of growth on isogenic strains showing susceptibility or intermediate level of resistance against glycopeptides. Altered susceptibility had emerged spontaneously after infection with a sensitive parental strain, thus not selected in vitro. This combined analysis allows the identification of hundreds of proteins considered, so far as hypothetical protein. In addition, this study provides not only a global picture of transcription and expression adaptations during a complex antibiotic resistance mechanism but also unravels potential drug targets or markers that are constitutively expressed by resistant strains regardless of their genetic background, amenable to be used as diagnostic targets. Keywords: Molecular markers, antibiotic resistance, glycopeptides, growth-phase

Dataset Information

N-glycopeptide Signatures in Liver Diseases

Publications

N-glycopeptide Signatures of IgA<sub>2</sub> in Serum from Patients with Hepatitis B Virus-related Liver Diseases.

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