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Loss of BCL9/9l suppresses Wnt driven tumourigenesis in models that recapitulate human cancer.

Abstract：

:Different thresholds of Wnt signalling are thought to drive stem cell maintenance, regeneration, differentiation and cancer. However, the principle that oncogenic Wnt signalling could be specifically targeted remains controversial. Here we examine the requirement of BCL9/9l, constituents of the Wnt-enhanceosome, for intestinal transformation following loss of the tumour suppressor APC. Although required for Lgr5+ intestinal stem cells and regeneration, Bcl9/9l deletion has no impact upon normal intestinal homeostasis. Loss of BCL9/9l suppressed many features of acute APC loss and subsequent Wnt pathway deregulation in vivo. This resulted in a level of Wnt pathway activation that favoured tumour initiation in the proximal small intestine (SI) and blocked tumour growth in the colon. Furthermore, Bcl9/9l deletion completely abrogated β-catenin driven intestinal and hepatocellular transformation. We speculate these results support the just-right hypothesis of Wnt-driven tumour formation. Importantly, loss of BCL9/9l is particularly effective at blocking colonic tumourigenesis and mutations that most resemble those that occur in human cancer.

journal_name

Nat Commun

journal_title

Nature communications

authors

Gay DM,Ridgway RA,Müller M,Hodder MC,Hedley A,Clark W,Leach JD,Jackstadt R,Nixon C,Huels DJ,Campbell AD,Bird TG,Sansom OJ

doi

10.1038/s41467-019-08586-3

subject

Has Abstract

pub_date

2019-02-13 00:00:00

pages

723

issue

1

issn

2041-1723

pii

10.1038/s41467-019-08586-3

journal_volume

10

pub_type

杂志文章

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