PXD044104 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | SAMD1 suppresses epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma. |
Description | SAMD1, a CpG island-binding protein, plays a pivotal role in the repression of its target genes by influencing the activity of KDM1A. Despite its significant correlation with outcomes in various tumor types, SAMD1's role in cancer has remained largely unexplored. In this study, we focus on pancreatic ductal adenocarcinoma (PDAC) and reveal that SAMD1 is a repressor of genes associated with epithelial-mesenchymal transition (EMT). Upon depletion of SAMD1 in PDAC cells, we observed significantly increased migration rates. Furthermore, high SAMD1 expression in PDAC patients correlated with lower expression of EMT signature genes and better prognosis, further underscoring its suppressive role. In-depth analysis revealed that SAMD1 exerts its effects by binding to specific genomic targets, including CDH2, encoding N-Cadherin, which emerged as a driver of enhanced migration upon SAMD1 knockout. Our investigations further demonstrated reduced chromatin-binding activity of SAMD1 in PDAC cells, prompting a search for regulatory mechanisms. This led to the discovery of the FBXO11-containing E3 ubiquitin ligase complex as a novel interactor of SAMD1, critically influencing its chromatin binding genome-wide. High FBXO11 expression in PDAC is associated with poor prognosis and increased expression of EMT-related genes, implying an antagonistic relationship between SAMD1 and FBXO11. In summary, our findings provide new insights into the regulation of EMT-related genes in PDAC, shedding light on the intricate role of SAMD1 and its interplay with FBXO11 in this particular cancer type. |
HostingRepository | PRIDE |
AnnounceDate | 2024-10-22 |
AnnouncementXML | Submission_2024-10-22_06:49:30.117.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | Ignasi Forne |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | No PTMs are included in the dataset |
Instrument | Q Exactive HF |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2023-07-26 08:08:47 | ID requested | |
1 | 2024-07-12 06:45:16 | announced | |
⏵ 2 | 2024-10-22 06:49:30 | announced | 2024-10-22: Updated project metadata. |
Publication List
Keyword List
submitter keyword: cancer, epithelial-mesenchymal transition, CpG islands, N-Cadherin, FBXO11, SAMD1, KDM1A, chromatin,pancreatic ductal adenocarcinoma |
Contact List
Dr. Robert |
contact affiliation | Institute of Molecular Biology and Tumor Research (IMT)Philipps University of Marburg, Marburg, 35043, Germany and Department of Hematology, Oncology, and Immunology, University Hospital Giessen and Marburg, Marburg, 35043, Germany |
contact email | robert.liefke@imt.uni-marburg.de |
lab head | |
Ignasi Forne |
contact affiliation | Biomedical Center-LMU |
contact email | ignasi.forne@lrz.uni-muenchen.de |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
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PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD044104
- Label: PRIDE project
- Name: SAMD1 suppresses epithelial-mesenchymal transition (EMT) in pancreatic ductal adenocarcinoma.