PXD043761 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | Tumour cells can escape antiproliferative pressure by type I interferon through immunoediting of interferon receptor expression |
Description | Type I interferons (IFNs) play a central role in innate immunity against virus infection, but also in the antitumour response. In tumour biology, an important mechanism of action apart from the more indirect immune-modulatory and anti-angiogenic effects of IFNs, is their direct impact on cell proliferation. Particularly for cancers arising in the context of chronic inflammation, constant exposure of cells to IFNs may constitute a strong selective pressure during tumour evolution. Expansion of tumour subclones or -populations that developed resistance to the antiproliferative effects of IFN might constitute an important contribution to immunoediting of the tumour leading to more aggressive and metastasising disease. Experimental evidence for this development of IFN-insensitivity has been scarce and its molecular mechanism is unclear. In this study we demonstrate that prolonged (six weeks) exposure of cells to IFN-β in vitro reduces their sensitivity to its antiproliferative effects, and that this phenotype was stable for up to four weeks. Furthermore, we observed substantial differences in cellular sensitivity to growth inhibition by IFN-β in a panel of ten different liver cancer cell lines of varying malignity. IFN-resistance was most prominent in a pair of highly dedifferentiated cell lines, and least in cells from well-differentiated tumours, fostering the hypothesis of IFN-driven immunoediting in advanced cancers. In both settings, long-term IFN selection in vitro as well as in dedifferentiated tumour cell lines, we found IFNAR expression to be substantially reduced, suggesting the receptor complex, in particular IFNAR2, to be a sensitive target amenable to immunoediting. Beyond new insights into possible molecular processes in tumour evolution, these findings might prove valuable for the development of biomarkers allowing to stratify tumours for their sensitivity to IFN treatment in the context of patient tailored therapies. |
HostingRepository | PRIDE |
AnnounceDate | 2024-10-22 |
AnnouncementXML | Submission_2024-10-22_06:15:29.825.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | Marcel Schilling |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | No PTMs are included in the dataset |
Instrument | Orbitrap Exploris 480 |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2023-07-13 07:16:40 | ID requested | |
1 | 2023-11-21 12:23:24 | announced | |
⏵ 2 | 2024-10-22 06:15:30 | announced | 2024-10-22: Updated project metadata. |
Publication List
Keyword List
submitter keyword: interferon signalling, immunoediting, cell proliferation, tumour evolution, liver cancer |
Contact List
Prof. Dr. Ursula Klingmüller |
contact affiliation | Division Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Heidelberg, Germany |
contact email | u.klingmueller@dkfz.de |
lab head | |
Marcel Schilling |
contact affiliation | Division Systems Biology of Signal Transduction, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg |
contact email | m.schilling@dkfz.de |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
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PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD043761
- Label: PRIDE project
- Name: Tumour cells can escape antiproliferative pressure by type I interferon through immunoediting of interferon receptor expression