Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomes of triple-negative breast cancer (TNBC) cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared

ABSTRACT: The expression levels of JMJD6 and its correlation with H2A.XY39ph differed in TNBC and non-TNBC cells. In addition, we have previously shown that H2A.XY39ph levels are positively correlated with tumor size, histological grade and advanced TNM stage in breast cancer. To analyze the role of JMJD6 in regulating the characteristics of different subtypes of breast cancer, the transcriptomes of TNBC cells (SUM159) and non-TNBC cells (HCC1569) that overexpressed JMJD6 were compared. We speculate that JMJD6 overexpression cause autophagy pathway activation in TNBC via enhancing ATG genes expression.

ORGANISM(S): Homo sapiens

SUBMITTER: Yan Liu

PROVIDER: E-MTAB-6517 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression of the IL-17/Th17 axis in the development of acute renal allograft rejection

Project description:Genesets for the IL-17 pathway and Th17 T-helper cell subtype showed increasing enrichment in 33 pre-transplant donor biopsies and 33 matching post-transplant biopsies from patients with increasing Banff grades of acute rejection (no signficant abnormalities, n=17; borderline, n=4; ARIA, n=7; ARIB, n=6) in gene set analysis using SAM (GSA, FDR 0.5; 1000 permutations, log rank regression) for a total of 3307 publically available and manually curated gene-sets. 14 genes of the IL-17 pathway gene-set and 132 genes of the Th17 gene set segregated patients according to their histological diagnosis by unsupervised hierarchical clustering and principal component analysis. This study demonstrates a significant role for the IL-17 pathway in the development of acute renal allograft rejection. Therapeutically targeting the IL-17 pathway presents a promising option in transplantation medicine and can be acchieved through drug reposittioning. Keywords: IL-17 pathway, drug repositioning, gene set enrichment analysis A total of 66 human renal allograft protocol biopsies were included in this study, 33 biopsies obtained at implantation prior to revascularization and 33 protocol biopsies obtained after transplantation. Whole genome expression profiles were assessed using microarrays. This dataset is part of the TransQST collection.

2014-01-01 | E-GEOD-34437 | biostudies-arrayexpress

Local regulation and clinical impact of complement gene expression in deceased and living donor kidney allografts

Project description:The biopsy samples obtained at implantation segregated in 2 distinct groups according to donor origin, with a cluster of 319 unique identified genes higher expressed in DD compared to LD kidneys, and 329 genes lower expressed (false discovery rate <5%). Using pathway analysis software a significant local renal overrepresentation of complement genes in DD implantation biopsies was identified. Complement gene expression in DD kidneys related both to donor death and cold ischemia duration, and was associated with a slower onset of renal allograft function. In post-transplantation protocol biopsies, there was a continued overexpression of complement genes, regardless of donor source. The local renal complement gene expression variability in post-transplantation biopsies correlated with renal graft function. This study demonstrates a significant and clinically relevant local overexpression of complement genes in DD kidneys at engraftment and continuous functionally important regulation of complement gene expression after transplantation, regardless of donor source. Targeted therapy interfering with complement activation is an attractive therapeutic target that deserves further investigation in solid organ transplantation. Keywords: time course, genomics gene expression A total of 95 human renal allograft protocol biopsies were included in this study, 28 biopsies (14 DD, 14 LD) obtained at implantation prior to revascularization and 67 protocol biopsies obtained after transplantation. Whole genome expression profiles were assessed using microarrays. This dataset is part of the TransQST collection.

2008-04-16 | E-GEOD-11166 | biostudies-arrayexpress

Transcriptome Shock Invokes Disruption of Parental Expression-Conserved Genes in Tetraploid Wheat

Project description:Allopolyploidy, entailing whole genome duplication (WGD) of merged divergent genomes of different species, often instigates transcriptome shock, whereby both total gene expression level and homeolog expression partitioning can be disrupted and remodeled. Little is known about the extent to which the parental expression-conserved genes will be disrupted/remodeled by allopolyploidization, nor the evolutionary relevancy of shock-induced expression repatterning. Here, by microarray-based gene expression profiling and gene-specific cDNA-pyrosequencing, we assessed transgenerational transcriptome shock in a synthetic allotetraploid wheat (AT2) with karyotype and basic morphology mimicking those of natural tetraploid wheat, Triticum turgidum. We show that the transcriptome shock in AT2 is exceptionally strong that it disrupted intrinsically conserved parental gene expression, and resulted in extensive expression nonadditivity in the newly formed allotetraploid plants. At total expression level, a substantial proportion of shock-induced novel expression, especially over-transgressive expression, was rapidly stabilized already in early generations of AT2. Extensive remodeling of homeolog expression occurred in AT2, including those genes that showed additive total expression, and which generated subgenome expression dominance, a pattern that mirrors T. turgidum. Thus, the shock-induced new patterns of gene expression at both the total expression level and subgenome homeolog partitioning showed evidence of evolutionary persistence. Complex relationships between homeolog expression remodeling and nonadditive total expression were observed in a tissue-specific manner. We have 9 samples including two tissues, leaf and young-inflorescence, respectively. Each sample has three replicates. So we overall have 54 samples.

2016-02-12 | E-GEOD-65844 | biostudies-arrayexpress

Heterogeneous CD3 expression levels in differing T-cell subsets account for in vivo anti-CD3-mediated immune resetting

Project description:The tolerogenic anti-CD3 monoclonal antibodies (anti-CD3) are promising compounds for the treatment of type 1 diabetes (T1D). Anti-CD3 administration induces transient T-cell depletion both in preclinical and in clinical studies. Notably, said depletion mainly affects CD4+ but not CD8+ T cells. Moreover, T1D reversal in preclinical models is accompanied by the selective expansion of CD4+FOXP3+ T regulatory (Treg) cells, which are fundamental for the long-term maintenance of anti-CD3-mediated tolerance. The mechanisms that lead to this immune-shaping by affecting mainly CD4+ T effector cells while sparing CD4+FOXP3+ Treg cells have still to be fully elucidated. This study shows that CD3 expression levels differ from one T-cell subset to another. CD4+FOXP3- T cells contain higher amounts of CD3 molecules than do CD4+FOXP3+ and CD8+ T cells both in mice and in humans. Said differences may explain the anti-CD3-mediated immune resetting that occurs in vivo after anti-CD3 administration in mice. In addition, transcriptome analysis demonstrates that CD4+FoxP3+ Treg cells are significantly less responsive than CD4+FoxP3- T cells to anti-CD3 treatment at molecular levels. Thus, heterogeneity in CD3 expression likely confers the various T-cell subsets differing susceptibility to in vivo tolerogenic anti-CD3-mediated modulation. This data sheds new light on the molecular mechanism that underlies anti-CD3-mediated immune resetting, and thus may open new opportunities to improve this promising treatment.

2015-01-19 | E-MTAB-2437 | biostudies-arrayexpress

Transcription profiling of genetically matched normal adjacent tissue, primary tumor and metastatic lymph-node to identify cancer and metastasis genes

Project description:Profiling of genetically matched normal adjacent tissue, primary tumor and metastatic lymph-node to identify cancer and metastasis genes.

2006-11-21 | E-MEXP-44 | biostudies-arrayexpress

microRNA profiling of luminal and TNBC breast cancer cell lines

Project description:two luminal cell lines were added, MCF7 and BT-474 two TNBC cell line were added, MB231 and BT-549 microRNA expression profiles were conpared between the luminal group and the TNBC group

2014-10-03 | E-GEOD-62022 | biostudies-arrayexpress

Comprehensive genomic analysis identify novel subtypes and targets of triple-negative breast cancer (198 TNBC tumors)

Project description:Recent meta-analyses suggest triple-negative breast cancer (TNBC) is a heterogenous disease. In this study we sought to define these TNBC subtypes and identify subtype-specific markers and targets. We identified and confirmed four distinct, stable TNBC subtypes: (1) Luminal-AR (LAR); 2) Mesenchymal (MES); 3) Basal-Like Immune-Suppressed (BLIS), and 4) Basal-Like Immune-Activated (BLIA). RNA profiling analysis was conducted on 198 TNBC tumors (ER-negativity defined as Allred Scale value â¤2) with >50% cellularity (discovery set: n=84; validation set: n=114)

2015-12-18 | E-GEOD-76124 | biostudies-arrayexpress

Human TNBC Cells 48h Treatment with OTSSP167 MELK Inhibitor vs. DMSO Control

Project description:Microarray comparing TNBC cells treated for 48 hours with OTSSp167 MELK Inhibitor and control (DMSO) Two-condition arrays: MDA-MB-231 cells were treated with either 4.5nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 48h. Two biological replicates, one per array, with a dye swap (technical replicate).

2017-05-01 | E-GEOD-68652 | biostudies-arrayexpress

Human TNBC Cells 72h Treatment with 45nM OTSSP167 MELK Inhibitor vs. DMSO Control

Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: MDA-MB-231 cells were treated with either 45nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

2017-05-01 | E-GEOD-68692 | biostudies-arrayexpress

Human TNBC Cells 72h Treatment with 4.5nM OTSSP167 MELK Inhibitor vs. DMSO Control

Project description:Microarray comparing TNBC cells treated for 72 hours with OTSSP167 MELK Inhibitor and control (DMSO) Two-condition arrays: MDA-MB-231 cells were treated with either 4.5nM OTSSP167 MELK Inhibitor or 0.045% DMSO for 72h. Two biological replicates, one per array, with a dye swap (technical replicate).

2017-05-01 | E-GEOD-68691 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data