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Integrative Multi-Omic characterization of LYN deficient HS-5 stroma cells

ABSTRACT: LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). To analyze the effect of LYN kinase on the leukemia supportive phenotype of the bone marrow stromal cell line HS-5, we generated single cell clones of LYN deficient cells. These cells were analyzed in a Multi-Omic approach, comprising four "Omic" layers [microarray-based transcriptome, label-free quantitative proteome and secretome, and SILAC-labelled phosphoproteome (phospho-tyrosine (pYome))] and analyzed integratively. Raw data of the single "Omic" layers are deposited in different repositories and linked below. The results of the data analysis for every "Omic" layer can be found in the spreadsheets below.

ORGANISM(S): Homo sapiens (human)

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PROVIDER: S-BSST703 | biostudies-other |

REPOSITORIES: biostudies-other

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Secretome of LYN deficient HS-5 stroma cells

Project description:LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). To analyze the effect of LYN kinase on the leukemia supportive phenotype of the bone marrow stromal cell line HS-5, we generated single cell clones of LYN deficient cells. These cells were analyzed in a Multi-Omic approach, including quantitative, label-free proteomic analysis of the Secretome.

2023-05-10 | PXD028855 | Pride

Transcriptome of LYN deficient HS-5 stroma cells

Project description:LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context-specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). To analyze the effect of LYN kinase on the leukemia supportive phenotype of the bone marrow stromal cell line HS-5, we generated single cell clones of LYN deficient stroma cells. These cells were analyzed in a Multi-Omic approach, including microarray based analysis of the transcriptome.

2023-01-01 | E-MTAB-10980 | biostudies-arrayexpress

Proteome / pYome of LYN deficient HS-5 stroma cells

2023-05-10 | PXD030582 | Pride

ATAC-Seq analysis of LYN deficient HS-5 stroma cells

2024-01-01 | E-MTAB-12531 | biostudies-arrayexpress

ATAC-Seq analysis of LYN deficient HS-5 stroma cells

Project description:ATAC-Seq analysis of LYN deficient HS-5 stroma cells

| PRJEB59002 | ENA

RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

2023-02-10 | E-MTAB-12629 | biostudies-arrayexpress

MOTA: Multi-omic integrative analysis for biomarker discovery.

Project description:Recent advancement of omic technologies provides researchers with opportunities to search for disease biomarkers at the systems level. However, selection of biomarker candidates from a large number of molecules involved at various layers of the biological system is challenging. In this paper, we propose multi-omic integrative analysis (MOTA), a network-based method that uses information from multi-omic data to identify candidate disease biomarkers. We evaluated the performance of MOTA in selecting disease-associated molecules from four sets of multi-omic data representing three cohorts of hepatocellular carcinoma (HCC) cases and patients with liver cirrhosis. The results demonstrate that MOTA leads to selection of more biomarker candidates that shared by two different cohorts compared to traditional statistical methods. Also, the networks constructed by MOTA allow users to investigate biological significance of the selected biomarker candidates.

| S-EPMC6986235 | biostudies-literature

RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

Project description:RNA-Seq analysis of LYN deficient HS-5 stroma cells cocultured with primary human CLL cells

| PRJEB59836 | ENA

Integrative multi-omic analysis reveals neurodevelopmental gene dysregulation in CIC-knockout and IDH1-mutant cells.

Project description:Capicua (CIC)'s transcriptional repressor function is implicated in neurodevelopment and in oligodendroglioma (ODG) aetiology. However, CIC's role in these contexts remains obscure, primarily from our currently limited knowledge regarding its biological functions. Moreover, CIC mutations in ODG invariably co-occur with a neomorphic IDH1/2 mutation, yet the functional relationship between these two genetic events is unknown. Here, we analysed models derived from an E6/E7/hTERT-immortalized (i.e. p53- and RB-deficient) normal human astrocyte cell line. To examine the consequences of CIC loss, we compared transcriptomic and epigenomic profiles between CIC wild-type and knockout cell lines, with and without mutant IDH1 expression. Our analyses revealed dysregulation of neurodevelopmental genes in association with CIC loss. CIC ChIP-seq was also performed to expand upon the currently limited ensemble of known CIC target genes. Among the newly identified direct CIC target genes were EPHA2 and ID1, whose functions are linked to neurodevelopment and the tumourigenicity of in vivo glioma tumour models. NFIA, a known mediator of gliogenesis, was discovered to be uniquely overexpressed in CIC-knockout cells expressing mutant IDH1-R132H protein. These results identify neurodevelopment and specific genes within this context as candidate targets through which CIC alterations may contribute to the progression of IDH-mutant gliomas. © 2021 The Authors. The Journal of Pathology published by John Wiley & Sons, Ltd on behalf of The Pathological Society of Great Britain and Ireland.

| S-EPMC9305137 | biostudies-literature

Integrative multi-omic profiling of adult mouse brain endothelial cells and potential implications in Alzheimer's disease.

Project description:The blood-brain barrier (BBB) is primarily manifested by a variety of physiological properties of brain endothelial cells (ECs), but the molecular foundation for these properties remains incompletely clear. Here, we generate a comprehensive molecular atlas of adult brain ECs using acutely purified mouse ECs and integrated multi-omics. Using RNA sequencing (RNA-seq) and proteomics, we identify the transcripts and proteins selectively enriched in brain ECs and demonstrate that they are partially correlated. Using single-cell RNA-seq, we dissect the molecular basis of functional heterogeneity of brain ECs. Using integrative epigenomics and transcriptomics, we determine that TCF/LEF, SOX, and ETS families are top-ranked transcription factors regulating the BBB. We then validate the identified brain-EC-enriched proteins and transcription factors in normal mouse and human brain tissue and assess their expression changes in mice with Alzheimer's disease. Overall, we present a valuable resource with broad implications for regulation of the BBB and treatment of neurological disorders.

| S-EPMC10843806 | biostudies-literature

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