Concomitant Notch activation and p53 deletion trigger epithelial-to-mesenchymal transition and metastasis in mouse gut.

Abstract:

:Epithelial-to-mesenchymal transition-like (EMT-like) is a critical process allowing initiation of metastases during tumour progression. Here, to investigate its role in intestinal cancer, we combine computational network-based and experimental approaches to create a mouse model with high metastatic potential. Construction and analysis of this network map depicting molecular mechanisms of EMT regulation based on the literature suggests that Notch activation and p53 deletion have a synergistic effect in activating EMT-like processes. To confirm this prediction, we generate transgenic mice by conditionally activating the Notch1 receptor and deleting p53 in the digestive epithelium (NICD/p53(-/-)). These mice develop metastatic tumours with high penetrance. Using GFP lineage tracing, we identify single malignant cells with mesenchymal features in primary and metastatic tumours in vivo. The development of such a model that recapitulates the cellular features observed in invasive human colorectal tumours is appealing for innovative drug discovery.

journal_name

Nat Commun

journal_title

Nature communications

authors

Chanrion M,Kuperstein I,Barrière C,El Marjou F,Cohen D,Vignjevic D,Stimmer L,Paul-Gilloteaux P,Bièche I,Tavares Sdos R,Boccia GF,Cacheux W,Meseure D,Fre S,Martignetti L,Legoix-Né P,Girard E,Fetler L,Barillot E,Louva

doi

10.1038/ncomms6005

subject

Has Abstract

pub_date

2014-10-08 00:00:00

pages

5005

issn

2041-1723

pii

ncomms6005

journal_volume

5

pub_type

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