Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Omics Analysis of Pancreatic Cancer Platelets Reveals Active “Education”, including Dysregulation of Splicing Signature and Inhibition of SPARC by Modified Forms of miRNAs

ABSTRACT: Omics Analysis of Pancreatic Cancer Platelets Reveals Active “Education”, including Dysregulation of Splicing Signature and Inhibition of SPARC by Modified Forms of miRNAs

PROVIDER: PRJNA672701 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Omics Analysis of Pancreatic Cancer Platelets Reveals Active “Education”, including Dysregulation of Splicing Signature and Inhibition of SPARC by Modified Forms of miRNAs

Project description:Pancreatic ductal adenocarcinoma (PDAC) is associated with hypercoagulation, but molecular mechanisms underlying PDAC/platelets interaction remain controversial. PDAC cells can activate platelets and change their RNA and protein content, thus, we performed an integrative study investigating the biological processes of differentially spliced mRNAs and expressed miRNAs, as well as proteins. To focus on these “dangerous liaisons”, we used benign disease as a background noise correction for putative inflammatory signals. Gene set enrichment analysis on differential miRNAs, RNA transcripts and proteins revealed an enrichment of RNA splicing, mRNA processing and translation initiation on miRNAs and proteins and depletion on RNA transcripts, as previously described. Moreover, correlation analyses revealed a specific regulation on SPARC RNA transcripts by isomiRs involved in cancer signaling, suggesting a specific modulation/”education” in PDAC platelets. We identified HBA1, HBD, CA1 and AGT as protein markers in PDAC platelets. In conclusion, our data show that platelets change their biological repertoire in the presence of PDAC, through dysregulation of miRNAs and splicing factors, supporting the presence of a clear de novo protein machinery that can “educate” the platelet.

2021-09-09 | PXD022514 | Pride

Omics Analysis of Pancreatic Cancer Platelets Reveals Active “Education”, including Dysregulation of Splicing Signature and Inhibition of SPARC by Modified Forms of miRNAs

Project description:PDAC cells can activate platelets and change their RNA and protein content, thus, we performed an integrative study investigating the biological processes of differentially spliced mRNAs and expressed miRNAs, as well as proteins. To focus on these “dangerous liaisons”, we used benign disease as a background noise correction for putative inflammatory signals. Gene set enrichment analysis on differential miRNAs, RNA transcripts and proteins revealed an enrichment of RNA splicing, mRNA processing and translation initiation on miRNAs and proteins and depletion on RNA transcripts, as previously described. Furthermore, we provide a new repertoire of PDAC and benign platelet-ome, visualized by the R shiny application, to be exploited for future studies. In conclusion, our data show that platelets change their biological repertoire in the presence of PDAC, through dysregulation of miRNAs and splicing factors, supporting the presence of de novo protein machinery that can “educate” the platelet. This has major clinical implications since the emerging molecules could provide important innovative PDAC biomarkers in the context of liquid biopsies.

2021-01-19 | GSE160252 | GEO

Modified forms of easyCLIP

Project description:Modified forms of easyCLIP

| PRJNA787947 | ENA

Specialized regulatory T cells control venous blood clot resolution through SPARC

Project description:The cells and mechanisms involved in blood clot resorption are only partially known. Regulatory T cells (Treg) accumulate in venous blood clots and regulate thrombolysis by controlling the recruitment, differentiation and matrix metalloproteinase (MMP) activity of monocytes. The clot Treg population is heterogeneous and contains a population of Treg that forms the matricellular acid- and cysteine-rich protein (SPARC). SPARC induces MMP activity in monocytes and SPARC+ Treg are required for clot resorption.

2023-06-01 | GSE155444 | GEO

SPARC knock down

Project description:SPARC knock down

| PRJNA327124 | ENA

Triple Negative Breast tumors: SPARC Positive Tumors vs SPARC Negative Tumors

Project description:The aim of this study was evaluate the transcriptome changes in the comparison between triple negative tumors with increased SPARC expression and triple negative tumors with decreased SPARC expression according to Nagai et al., 2011 (Breast Cancer Res Treat (2011) 126:1–14) The results generated could be of particular interest to better define the prognostic impact of SPARC expression in triple negative breast tumors

2018-07-01 | GSE98931 | GEO

Platelets orchestrate the resolution of pulmonary inflammation in mice through Treg repositioning and macrophage education

Project description:Our study investigates how interactions of platelets with regulatory T cells (Tregs) modulates the transcriptomic profile of Tregs and pro- and anti-inflammatory macrophages in the lung during resolution of pulmonary inflammation.

2021-04-14 | GSE171989 | GEO

Platelets orchestrate the resolution of pulmonary inflammation in mice through Treg repositioning and macrophage education

Project description:Platelets orchestrate the resolution of pulmonary inflammation in mice through Treg repositioning and macrophage education

| PRJNA721629 | ENA

SPARC-null vs. wild-type lens epithelium

Project description:SPARC is a matricellular glycoprotein involved in regulation of the extracellular matrix, growth factors, adhesion, and migration. SPARC-null mice have altered basement membranes and develop posterior sub-capsular cataracts with cell swelling and equatorial vacuoles. Exchange of fluid, nutrients, and waste products in the avascular lens is driven by a unique circulating ion current. Here we demonstrate that SPARC-null mouse lenses exhibit abnormal circulation of fluid, ion, and small molecules which leads to altered fluorescein distribution in vivo, loss of resting membrane polarization, and altered distribution of small molecules. Microarray analysis of SPARC-null lenses showed changes in gene expression of ion channels and receptors, matrix and adhesion genes, cytoskeleton, immune response genes, and cell signaling molecules. Our results demonstrate that the regulation of SPARC on cell-capsular matrix interactions can influence the circulation of fluid and ions in the lens, and the phenotype in the SPARC-null mouse lens is the result of multiple intersecting pathways.

2009-05-01 | GSE13402 | GEO

Transcription profiling of mouse SPARC-null vs. wild-type lens epithelium

2009-05-11 | E-GEOD-13402 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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