Faculty Collaboration Database

Homotypic cell cannibalism, a cell-death process regulated by the nuclear protein 1, opposes to metastasis in pancreatic cancer. EMBO Mol Med 2012 Sep;4(9):964-79

Date

07/24/2012

Pubmed ID

22821859

Pubmed Central ID

PMC3491828

DOI

10.1002/emmm.201201255

Scopus ID

2-s2.0-84863201071 (requires institutional sign-in at Scopus site)   63 Citations

Abstract

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 β. 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.

Author List

Cano CE, Sandí MJ, Hamidi T, Calvo EL, Turrini O, Bartholin L, Loncle C, Secq V, Garcia S, Lomberk G, Kroemer G, Urrutia R, Iovanna JL

Authors

Gwen Lomberk PhD Professor in the Surgery department at Medical College of Wisconsin
Raul A. Urrutia MD Center Director, Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adenocarcinoma
Aged
Aged, 80 and over
Animals
Basic Helix-Loop-Helix Transcription Factors
Cell Death
Cytophagocytosis
Female
Humans
Male
Mice
Middle Aged
Neoplasm Metastasis
Neoplasm Proteins
Pancreatic Neoplasms