GSE160252
Omics Analysis of Pancreatic Cancer Platelets Reveals Active “Education”, including Dysregulation of Splicing Signature and Inhibition of SPARC by Modified Forms of miRNAs
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. Overall design: examination of molecular mechanisms in PDAC and Benign blood platelets