clear factor 4 alpha in medulloblastoma biology, which we attempted to inhibit with a known drug inhibitor, MEDICA 
16. Instead, this resulted in an increase in D283MED cell proliferation, suggesting that the transcription factor may actually be a tumor suppressor in at least this cell line. To our knowledge this is the first report of characterizations and functional delineations of medulloblastoma exosomes, and the first to suggest a role for HNF4A in medulloblastoma biology. The exosome proteome has received extensive study, revealing sets of common proteins, canonical proteins, and those unique to particular 62717-42-4 site exosomes based on their cells of origin. Many of these have been cataloged in the ExoCarta website. With that database as a reference, our results show nearly a 65% overlap in protein identity, with the rest appearing unique. Our classifications showed relatively high percentages of nuclear proteins, but also substantial amounts of proteins involved in transcriptional regulation and with nucleic acid binding properties. The classifications may be somewhat artificial, since as mentioned, proteins like the HSPs appear in multiple subcellular locations. Also, CENPE, a kinetochore protein linking chromatin to microtubules, is considered a nuclear protein, even tho at that point in the cell cycle the nucleus has broken down. The Cullins may associate in complexes with potential nuclear localization, but are not necessarily themselves nuclear localized. Heterogeneous ribonuclear proteins are also known to cell surface localize. Thus, rigid classifications may be futile. The exosome proteome has more often than not been utilized to predict disease biomarkers rather than to predict functional activities of the vesicles. Our own work here with patient serum exosomes implies that GPNMB and/or ERBB2 may be tumor-specific exosome markers. Indeed, one lament in the area of brain tumor proteomics has been the lack of functional association with proteomic data. Herein we showed that exosome biology can derive from analyses of the proteome, demonstrating and validating that tumor-derived exosomes may enhance proliferation of tumor cells, which has been demonstrated previously. This is important because tumor-derived, exosome-like vesicles have been shown to induce apoptosis in a pancreatic cancer cell line, so the effects of extracellular vesicles may vary depending on the microvesicles and perhaps the recipient cells. Exosome-driven migration of endothelial cells has been shown for exosomes of tumor and cardiomyocite progenitor origins, as well as cancer cell exosomes promoting cancer cell migration with an implication for extracellular HSP90, and RAB GTPases. Our proteomic analysis also suggested a role for L1-NCAM, which has a cleaved form found extracellularly and in exosomes, but appears full-length in D283MED exosomes and in another brain tumor cell line where it plays a role in cell motility. Platelet-derived exosomes/microvesicles also have migratory attractant properties towards tumor cells, and the vesicles induce MMP activities in recipient cells. Tumor cells themselves secrete active MMPs in exosomes, and other brain tumor exosomes possess active MMPs. Our results here suggest that exosomes may play an important role PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/22203983 in attracting or ��leading the way��for medulloblastoma migration; given that the D283MED cell line is not considered very adherent, much less highly migratory in culture Functional Roles of Medulloblastoma Exosomes 10 Fun
