D the alterations observed in astrocyte migration, we performed comprehensive quantitative MS-based proteomics. Making use of Ingenuity Pathway Analysis, an interaction network was generated from differentially abundant proteins and upstream regulators. Predicted modifications in activation states were tested by qPCR. Results: We observed a considerable boost in podosome/invadopodia formation and Cy3-gelatin degradation by the regular astrocytes in response to the GBM stem- and GBM differentiated-EVs, with GBM stem-EVs eliciting a higher impact on the astrocytes. A lot more than 1650 proteins have been identified and quantified by mass spectrometry and bioinformatics predicted an upstream activation of FN1 and TGFB1 and inhibition of p53 in normal astrocytes exposed to GBM-EVs. qPCR research confirmed predicted increases in RNA levels of FN1 and TGFB1 along with a decrease in TP53 in GBM-EV exposed astrocytes. Summary/Conclusion: The inhibition of TP53 signalling as well as the activation of FN1 and TGFB1 in standard astrocytes may be a mechanism by which GBM manipulates normal astrocytes to acquire a cancerous phenotype and aid GBM malignancy.ISEV 2018 abstract bookPS07.Part of CD158a/KIR2DL1 Proteins web exosomes in inducing neuroendocrine differentiation in advanced prostate cancer Sharanjot Saini; Divya Bhagirath; Thao Yang; Shahana Majid; Rajvir Dahiya; Yuichiro Tanaka SFVAMC and UCSF, San Francisco, USAPS07.18 = OWP1.Cancer-derived extracellular vesicles facilitate osteoclast fusion and differentiation through enhancing filopodia formation in osteoclast precursorsPS07.Distinctive expression patterns of exosomal miRNAs under Cyclosporin A and Rapamycin treatment in distinct aggressiveness colorectal carcinomas Valeria Tubita1; Maria Jose Ramirez-Bajo2; Juan Jose Lozano3; Daniel Moya Rull4; Jordi Rovira1; Elisenda Banon-Maneus2; Josep M Campistol5; Fritz Diekmann5; Ignacio Revuelta5 IDIBAPS, Barcelona, Spain; 2FundaciCl ic per a La Recerca, Barcelona, Spain; CIBEREHD, Barcelona, Spain; 4Laboratori Experimental de Nefrologia i Trasplantament (LENIT), Barcelona, Spain; 5Hospital Cl ic de Barcelona, Barcelona, Spain1Background: Neuroendocrine prostate cancer (NEPC) is definitely an aggressive variant of sophisticated prostate cancer (PCa) present in 30 of metastatic castration-resistant tumours, generally emerging because of this of AR-targeted therapies for instance enzalutamide, by means of neuroendocrine differentiation (NED). Owing to NED, tumours show neuroendocrine (NE) characteristics using the expression of neuronal markers for example enolase 2 (ENO2), chromogranin A (CHGA) and synaptophysin (SYP). Clinically, NEPC manifests as the presence of visceral metastatic disease, low serum PSA levels relative to illness burden and restricted response to AR signalling inhibitors. The molecular basis of NED/NEPC is poorly understood. We propose that as well as cell intrinsic genetic determinants of NED, tumour exosomes are critical to facilitate neuroendocrine differentiation of prostate tumours via horizontal transfer of functional NE aspects and regulatory microRNAs (miRNAs) to recipient cells. Techniques: Exosomes have been isolated from cell culture Serine/Threonine Kinase 3 Proteins Molecular Weight models of PCa NED followed by (i) modest RNA-next generation sequencing (NGS) and (ii) Western blot analyses for oncogenic variables to identify novel regulators that play a function in exosome-mediated intercellular communication underlying NED. Exosome isolation reagent was utilised for exosome isolation as per manufacturer’s guidelines. The integrity of exosomal preparations was confirmed by nanoparticle tracking analysis.