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ROS production and NF-κB activation triggered by RAC1 facilitate WNT-driven intestinal stem cell proliferation and colorectal cancer initiation.

Abstract：

:The Adenomatous Polyposis Coli (APC) gene is mutated in the majority of colorectal cancers (CRCs). Loss of APC leads to constitutively active WNT signaling, hyperproliferation, and tumorigenesis. Identification of pathways that facilitate tumorigenesis after APC loss is important for therapeutic development. Here, we show that RAC1 is a critical mediator of tumorigenesis after APC loss. We find that RAC1 is required for expansion of the LGR5 intestinal stem cell (ISC) signature, progenitor hyperproliferation, and transformation. Mechanistically, RAC1-driven ROS and NF-κB signaling mediate these processes. Together, these data highlight that ROS production and NF-κB activation triggered by RAC1 are critical events in CRC initiation.

journal_name

Cell Stem Cell

journal_title

Cell stem cell

authors

Myant KB,Cammareri P,McGhee EJ,Ridgway RA,Huels DJ,Cordero JB,Schwitalla S,Kalna G,Ogg EL,Athineos D,Timpson P,Vidal M,Murray GI,Greten FR,Anderson KI,Sansom OJ

doi

10.1016/j.stem.2013.04.006

subject

Has Abstract

pub_date

2013-06-06 00:00:00

pages

761-73

issue

6

eissn

1934-5909

issn

1875-9777

pii

S1934-5909(13)00142-2

journal_volume

12

pub_type

杂志文章

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