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PXD007721-1

PXD007721 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitleCharacterization of syntenin knockout exosomes from 4T1 murine breast cancer cells
DescriptionTumor cells are known to induce tumor-supporting phenotypes in surrounding stroma cells which leads to the creation of a favourable tumor niche and sustained growth as well as progression of the tumor. One mechanism how tumor cells can modulate surrounding stroma cells is through the release of extracellular vesicles. These vesicles comprise large plasma membrane-derived microvesicles (diameter 100-1000 nm) as well as the better characterized smaller exosomes (diameter <100 nm) which are derived from intraluminal vesicles inside endosomal compartments. In spite of the identification of vesicle-mediated tumor-tumor and tumor-stroma intracellular communication loops, the tumor-supporting factors present on tumor vesicles as well as the factors that regulate their export are largely unknown. One attractive candidate protein which could be involved in controlling vesicular cargo selection is the adaptor scaffolding protein syntenin/SDCBP, which is known as a marker protein highly expressed on exosomes. Syntenin is characterized by two structural protein interaction modules, the PDZ domains, which can either bind to other PDZ domains or to the C-terminus of target proteins in a sequence-specific way, thereby enabling protein-protein interactions. PDZ proteins in general are known to be involved in the recruitment and assembly of specific protein complexes, especially at the cellular plasma membrane. Syntenin is a factor that has been shown to control not only the biogenesis of exosomes, but also the sorting of specific proteins to these vesicles. While it is highly expressed in human fetal tissues, its expression is significantly downregulated in adult tissues with the exception of the heart or placenta. However, high levels of syntenin seem to be restored in advanced human cancer of different entities and thereby suggest a role for syntenin in tumor progression. Previous results from the group of Pascale Zimmermann showed that syntenin is of particular importance for regulating the sorting of its (known) target proteins to exosomes which would allow their distribution to neighboring stroma cells. To analyze which tumor-supporting factors are present on breast cancer exosomes and which of them are regulated by syntenin, exosomes from 4T1 wildtype cells (syntenin-high) and from two clones of syntenin CRISPR/Cas9 syntenin knockout cells were isolated from cell culture supernatants by differential ultracentrifugation and then analyzed and compared by label-free mass spectrometry.
HostingRepositoryPRIDE
AnnounceDate2025-08-25
AnnouncementXMLSubmission_2025-08-24_17:52:55.428.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterLuc Camoin
SpeciesList scientific name: Mus musculus (Mouse); NCBI TaxID: 10090; scientific name: Bos taurus (Bovine); NCBI TaxID: 9913;
ModificationListmonohydroxylated residue; iodoacetamide derivatized residue
InstrumentQ Exactive
Dataset History
RevisionDatetimeStatusChangeLog Entry
02017-09-12 01:59:42ID requested
12025-08-24 17:52:56announced
Publication List
Irmer B, Angenendt A, Camoin L, Audebert S, Geyer C, Gerwing M, Spiessbach H, Hebel M, Baudelet É, Wlochowitz D, Hansen U, Bleckmann A, Zimmermann P, Menck K, Syntenin Controls Extracellular Vesicle-Induced Tumour Migration by Regulating the Expression of Adhesion Proteins on Small Extracellular Vesicles. J Extracell Vesicles, 14(8):e70133(2025) [pubmed]
10.1002/jev2.70133;
Keyword List
curator keyword: Biological, Biomedical
submitter keyword: breast cancer, syntenin, CRISPR/Cas9,Exosomes
Contact List
Luc Camoin
contact affiliationMarseille proteomique, Inserm U1068, CNRS UMR 7258, Aix marseille University UM105
contact emailluc.camoin@inserm.fr
lab head
Luc Camoin
contact affiliationLife Sciences
contact emailluc.camoin@inserm.fr
dataset submitter
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Dataset FTP location
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