Journal
EMBO MOLECULAR MEDICINE
Volume 4, Issue 9, Pages 964-979Publisher
WILEY-BLACKWELL
DOI: 10.1002/emmm.201201255
Keywords
cell cannibalism; metastasis; Nupr1; pancreatic cancer; TGF ss
Categories
Funding
- La Ligue Contre le Cancer
- INCa, Canceropole PACA
- INSERM
- NIH [DK52913]
- The Mayo Clinic Center for Cell Signaling in Gastroenterology [NIDDK P30DK084567]
- La Ligue
- l'Association pour la Recherche sur le Cancer
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Pancreatic adenocarcinoma (PDAC) is an extremely deadly disease for which all treatments available have failed to improve life expectancy significantly. This may be explained by the high metastatic potential of PDAC cells, which results from their dedifferentiation towards a mesenchymal phenotype. Some PDAC present cell-in-cell structures whose origin and significance are currently unknown. We show here that cell-in-cells form after homotypic cell cannibalism (HoCC). We found PDAC patients whose tumours display HoCC develop less metastasis than those without. In vitro, HoCC was promoted by inactivation of the nuclear protein 1 (Nupr1), and was enhanced by treatment with transforming growth factor beta. HoCC ends with death of PDAC cells, consistent with a metastasis suppressor role for this phenomenon. Hence, our data indicates a protective role for HoCC in PDAC and identifies Nupr1 as a molecular regulator of this process.
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