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http://hdl.handle.net/2445/196615
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DC Field | Value | Language |
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dc.contributor.author | Favaro, Francesca | - |
dc.contributor.author | Both, Demi | - |
dc.contributor.author | Derks, Ingrid A. M. | - |
dc.contributor.author | Spaargaren, Marcel | - |
dc.contributor.author | Muñoz Pinedo, Cristina | - |
dc.contributor.author | Eldering, Eric | - |
dc.date.accessioned | 2023-04-12T11:10:41Z | - |
dc.date.available | 2023-04-12T11:10:41Z | - |
dc.date.issued | 2023-02-08 | - |
dc.identifier.issn | 2157-9024 | - |
dc.identifier.uri | http://hdl.handle.net/2445/196615 | - |
dc.description.abstract | Impairments in protein folding in the endoplasmic reticulum (ER) lead to a condition called ER stress, which can trigger apoptosis via the mitochondrial or the death receptor (extrinsic) pathway. There is controversy concerning involvement of the death receptor (DR)4 and DR5-Caspase-8 -Bid pathway in ER stress-mediated cell death, and this axis has not been fully studied in B-cell malignancies. Using three B-cell lines from Mantle Cell Lymphoma, Waldenstrom's macroglobulinemia and Multiple Myeloma origins, we engineered a set of CRISPR KOs of key components of these cell death pathways to address this controversy. We demonstrate that DR4 and/or DR5 are essential for killing via TRAIL, however, they were dispensable for ER-stress induced-cell death, by Thapsigargin, Brefeldin A or Bortezomib, as were Caspase-8 and Bid. In contrast, the deficiency of Bax and Bak fully protected from ER stressors. Caspase-8 and Bid were cleaved upon ER-stress stimulation, but this was DR4/5 independent and rather a result of mitochondrial-induced feedback loop subsequent to Bax/Bak activation. Finally, combined activation of the ER-stress and TRAIL cell-death pathways was synergistic with putative clinical relevance for B-cell malignancies. | - |
dc.format.extent | 9 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Springer Science and Business Media LLC | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1038/s41389-023-00450-w | - |
dc.relation.ispartof | Oncogenesis, 2023, vol. 12, num. 1, p. 6 | - |
dc.relation.uri | https://doi.org/10.1038/s41389-023-00450-w | - |
dc.rights | cc by (c) Favaro, Francesca et al., 2023 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.source | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) | - |
dc.subject.classification | Limfomes | - |
dc.subject.classification | Apoptosi | - |
dc.subject.classification | Expressió gènica | - |
dc.subject.other | Lymphomas | - |
dc.subject.other | Apoptosis | - |
dc.subject.other | Gene expression | - |
dc.title | Negligible role of TRAIL death receptors in cell death upon endoplasmic reticulum stress in B-cell malignancies | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2023-04-11T14:42:08Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 36755015 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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s41389-023-00450-w.pdf | 2.59 MB | Adobe PDF | View/Open |
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