PXD054295 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | Secretomes from non-small cell lung cancer cells induce endothelial plasticity through a partial endothelial-to-mesenchymal transition |
Description | The tumor microenvironment (TME) of non-small cell lung cancer (NSCLC) is highly heterogeneous and is involved in tumorigenesis and resistance to therapy. Among the cells of the TME, endothelial cells are associated with the latter processes through endothelial-to-mesenchymal transition (EndMT). During EndMT, endothelial cells (ECs) progressively lose their endothelial phenotype in favor of a mesenchymal phenotype, which favors the production of cancer-associated fibroblasts. Our study aimed to investigate the consequences of exposure to different lung tumor secretomes on EC phenotype and plasticity. Conditioned media (CM) were prepared from the tumor cell lines A549, H1755, H23, H1437 and H1975. Proliferation and migration of endothelial cells treated with these CMs were assessed by Cyquant® and Incucyte® technologies, respectively. The angiogenic capacity of ECs was assessed by following tubulogenesis on Matrigel®. Phenotypic changes in treated ECs were detected by flow cytometry. Morphological analysis of actin fibers was performed by immunohistochemistry, while proteomic analysis by mass spectrometry was used to identify the protein content of secretomes. A change of the endothelial phenotype was found when HUVECs were treated with different CMs. This phenotypic change was associated with a morphological change, an increase in both stress fiber expression and spontaneous migration. Furthermore, an increase in mesenchymal markers (±-SMA and CD44) confirmed the phenotypic changes. However, the secretomes did not modify the rate of double-labelled cells (vWF+/-SMA+ or CD31+/CD44+). Proteomic analysis identified potential targets involved in the EndMT with therapeutic relevance. Taken together, these data suggest that CMs are capable of inducing partial EndMT. |
HostingRepository | PRIDE |
AnnounceDate | 2025-04-24 |
AnnouncementXML | Submission_2025-04-24_02:11:02.178.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | François Guillonneau |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | monomethylated residue; monohydroxylated residue |
Instrument | timsTOF Pro 2 |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2024-07-27 03:28:15 | ID requested | |
⏵ 1 | 2025-04-24 02:11:03 | announced | |
Publication List
Bourreau C, Navarro E, Cotinat M, Krejbich M, Guillonneau F, Guette C, Boissard A, Henry C, Corre I, Treps L, Clere N, Secretomes From Non-Small Cell Lung Cancer Cells Induce Endothelial Plasticity Through a Partial Endothelial-to-Mesenchymal Transition. Cancer Med, 14(5):e70707(2025) [pubmed] |
10.1002/cam4.70707; |
Keyword List
submitter keyword: Human, EMT, DIA-PASEF, non-small cell, lung cancer, secretome |
Contact List
Nicolas Clere |
contact affiliation | MINT UMR Inserm 1066 CNRS 6021 IBS IRIS CHU 4 rue Larrey F-49933 ANGERS France |
contact email | nicolas.clere@univ-angers.fr |
lab head | |
François Guillonneau |
contact affiliation | Institut de Cancerologie de l'Ouest (ICO) Angers |
contact email | francois.guillonneau@inserm.fr |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2025/04/PXD054295 |
PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD054295
- Label: PRIDE project
- Name: Secretomes from non-small cell lung cancer cells induce endothelial plasticity through a partial endothelial-to-mesenchymal transition