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Loss of p53 in enterocytes generates an inflammatory microenvironment enabling invasion and lymph node metastasis of carcinogen-induced colorectal tumors.

Abstract：

:Loss of p53 is considered to allow progression of colorectal tumors from the adenoma to the carcinoma stage. Using mice with an intestinal epithelial cell (IEC)-specific p53 deletion, we demonstrate that loss of p53 alone is insufficient to initiate intestinal tumorigenesis but markedly enhances carcinogen-induced tumor incidence and leads to invasive cancer and lymph node metastasis. Whereas p53 controls DNA damage and IEC survival during the initiation stage, loss of p53 during tumor progression is associated with increased intestinal permeability, causing formation of an NF-κB-dependent inflammatory microenvironment and the induction of epithelial-mesenchymal transition. Thus, we propose a p53-controlled tumor-suppressive function that is independent of its well-established role in cell-cycle regulation, apoptosis, and senescence.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Schwitalla S,Ziegler PK,Horst D,Becker V,Kerle I,Begus-Nahrmann Y,Lechel A,Rudolph KL,Langer R,Slotta-Huspenina J,Bader FG,Prazeres da Costa O,Neurath MF,Meining A,Kirchner T,Greten FR

doi

10.1016/j.ccr.2012.11.014

subject

Has Abstract

pub_date

2013-01-14 00:00:00

pages

93-106

issue

1

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(12)00493-X

journal_volume

23

pub_type

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