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dc.contributor.author
Hamidi, Tewfik
dc.contributor.author
Algül, Hana
dc.contributor.author
Cano, Carla Eliana
dc.contributor.author
Sandi, Maria José
dc.contributor.author
Molejon, Maria Ines
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dc.contributor.author
Riemann, Marc
dc.contributor.author
Calvo, Ezequiel Luis
dc.contributor.author
Lomberk, Gwen
dc.contributor.author
Dagorn, Jean Charles
dc.contributor.author
Weih, Falk
dc.contributor.author
Urrutia, Raul
dc.contributor.author
Schmid, Roland Michael
dc.contributor.author
Iovanna, Juan Lucio
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dc.date.available
2023-10-31T12:12:22Z
dc.date.issued
2012-06
dc.identifier.citation
Hamidi, Tewfik; Algül, Hana; Cano, Carla Eliana; Sandi, Maria José; Molejon, Maria Ines; et al.; Nuclear protein 1 promotes pancreatic cancer development and protects cells from stress by inhibiting apoptosis; American Society for Clinical Investigation; Journal of Clinical Investigation; 122; 6; 6-2012; 2092-2103
dc.identifier.issn
0021-9738
dc.identifier.uri
http://hdl.handle.net/11336/216511
dc.description.abstract
Pancreatic ductal adenocarcinoma (PDAC) has the lowest survival rate of all cancers and shows remarkable resistance to cell stress. Nuclear protein 1 (Nupr1), which mediates stress response in the pancreas, is frequently upregulated in pancreatic cancer. Here, we report that Nupr1 plays an essential role in pancreatic tumorigenesis. In a mouse model of pancreatic cancer with constitutively expressed oncogenic KrasG12D, we found that loss of Nupr1 protected from the development of pancreatic intraepithelial neoplasias (PanINs). Further, in cultured pancreatic cells, nutrient deprivation activated Nupr1 expression, which we found to be required for cell survival. We found that Nupr1 protected cells from stress-induced death by inhibiting apoptosis through a pathway dependent on transcription factor RelB and immediate early response 3 (IER3). NUPR1, RELB, and IER3 proteins were coexpressed in mouse PanINs from KrasG12D-expressing pancreas. Moreover, pancreasspecific deletion of Relb in a KrasG12D background resulted in delayed in PanIN development associated with a lack of IER3 expression. Thus, efficient PanIN formation was dependent on the expression of Nupr1 and Relb, with likely involvement of IER3. Finally, in patients with PDAC, expression of NUPR1, RELB, and IER3 was significantly correlated with a poor prognosis. Cumulatively, these results reveal a NUPR1/RELB/IER3 stress-related pathway that is required for oncogenic KrasG12D-dependent transformation of the pancreas.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Society for Clinical Investigation
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Nupr1
dc.subject
Pancreatic Cancer
dc.subject
Pancreas
dc.subject
Apoptosis
dc.subject.classification
Gastroenterología y Hepatología
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dc.subject.classification
Medicina Clínica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Nuclear protein 1 promotes pancreatic cancer development and protects cells from stress by inhibiting apoptosis
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2023-04-19T17:28:30Z
dc.journal.volume
122
dc.journal.number
6
dc.journal.pagination
2092-2103
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Ann Arbor, Michigan
dc.description.fil
Fil: Hamidi, Tewfik. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia
dc.description.fil
Fil: Algül, Hana. Technical University of Munich; Alemania
dc.description.fil
Fil: Cano, Carla Eliana. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia
dc.description.fil
Fil: Sandi, Maria José. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia
dc.description.fil
Fil: Molejon, Maria Ines. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Riemann, Marc. Leibniz-Institut für Altersforschung; Alemania
dc.description.fil
Fil: Calvo, Ezequiel Luis. Molecular Endocrinology and Oncology Research Center; Canadá
dc.description.fil
Fil: Lomberk, Gwen. Laboratory of Epigenetics and Chromatin Dynamics; Estados Unidos
dc.description.fil
Fil: Dagorn, Jean Charles. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia
dc.description.fil
Fil: Weih, Falk. Leibniz-Institut für Altersforschung; Alemania
dc.description.fil
Fil: Urrutia, Raul. Laboratory of Epigenetics and Chromatin Dynamics; Estados Unidos
dc.description.fil
Fil: Schmid, Roland Michael. Technical University of Munich; Alemania
dc.description.fil
Fil: Iovanna, Juan Lucio. Centre de Recherche En Cancérologie de Marseille; Francia. Inserm; Francia. Aix-Marseille Université; Francia
dc.journal.title
Journal of Clinical Investigation
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1172/jci60144
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366404/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/60144
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