⮝ Full datasets listing
PXD073617
PXD073617 is an original dataset announced via ProteomeXchange.
Dataset Summary
| Title | Metabolic plasticity and optimal redox homeostasis are essential for efficient metastatic colonization |
| Description | Cancer cells must dynamically reprogram their metabolism to adapt to changing microenvironmental conditions during tumor growth and metastatic dissemination. This results in metabolic flexibility and plasticity, allowing the use of multiple metabolic routes. Metastasis of solid tumors, the principal cause of cancer-related mortality, is driven by cellular plasticity often through activation of an epithelial-mesenchymal transition (EMT). These processes are regulated by the transcription factor ZEB1, which is frequently upregulated during tumor progression. To investigate the role of metabolic plasticity in metastasis, we employed murine pancreatic ductal adenocarcinoma (PDAC) cell lines with distinct EMT states and lung colonization capacities. Highly plastic epithelial-type cancer cells (KPCepi) efficiently colonized the lung, whereas ZEB1-deficient cancer cells (KPCZ) lost their plasticity and showed markedly reduced colonization. This defect correlated with impaired glycolytic reserve, mitochondrial dysfunction, as well as reduced levels of detoxifying metabolites, including NADPH and reduced glutathione. Interestingly mesenchymal-type cancer cells (KPCmes) also exhibited poor lung colonization despite retaining normal glycolytic capacity and a high proportion of functional mitochondria; however, similar to KPCZ cells, they displayed diminished levels of detoxifying metabolites. Both KPCZ and KPCmes cells with low metastatic capacity were more susceptible to ferroptosis, indicating a limited ability to counteract reactive oxygen species under stress. Together, these findings demonstrate that metabolic plasticity and redox homeostasis are essential prerequisites for efficient lung colonization, and suggest that concurrent targeting of metabolic adaptability and redox buffering may represent a promising strategy to prevent metastasis in aggressive PDAC tumors. |
| HostingRepository | MassIVE |
| AnnounceDate | 2026-06-01 |
| AnnouncementXML | Submission_2026-06-01_04:51:54.536.xml |
| DigitalObjectIdentifier | |
| ReviewLevel | Non peer-reviewed dataset |
| DatasetOrigin | Original dataset |
| RepositorySupport | Unsupported dataset by repository |
| PrimarySubmitter | Witold Szymanski |
| SpeciesList | scientific name: Mus musculus; common name: house mouse; NCBI TaxID: 10090; |
| ModificationList | Acetyl; Carbamidomethyl |
| Instrument | timsTOF Pro |
Dataset History
| Revision | Datetime | Status | ChangeLog Entry |
|---|---|---|---|
| 0 | 2026-01-26 22:51:52 | ID requested | |
| ⏵ 1 | 2026-06-01 04:51:55 | announced |
Publication List
| no publication |
Keyword List
| submitter keyword: Cancer, metastasis, metabolism, cellular plasticity, glycolysis, mitochondria, redox, epithelial-to-mesenchymal transition, DatasetType:Proteomics |
Contact List
| Marc Stemmler | |
|---|---|
| contact affiliation | Department of Experimental Medicine I, FAU University Erlangen-Nuernberg, Erlangen |
| contact email | marc.stemmler@fau.de |
| lab head | |
| Witold Szymanski | |
| contact affiliation | Philipps-University Marburg Biochemical/Pharmacological Center Department of Medicine |
| contact email | witold.szymanski@uni-marburg.de |
| dataset submitter | |
Full Dataset Link List
| MassIVE dataset URI |
| 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://massive-ftp.ucsd.edu/v12/MSV000100598/ |
