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Mutant Ras and inflammation-driven skin tumorigenesis is suppressed via a JNK-iASPP-AP1 axis

Abstract:

Concurrent mutation of a RAS oncogene and the tumor suppressor p53 is common in tumorigenesis, and inflammation can promote RAS-driven tumorigenesis without the need to mutate p53. Here, we show, using a well-established mutant RAS and an inflammation-driven mouse skin tumor model, that loss of the p53 inhibitor iASPP facilitates tumorigenesis. Specifically, iASPP regulates expression of a subset of p63 and AP1 targets, including genes involved in skin differentiation and inflammation, sugges...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1016/j.celrep.2022.111503

Authors


More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
ORCID:
0000-0001-9753-2385
More by this author
Role:
Author
ORCID:
0000-0002-2144-583X
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
ORCID:
0000-0002-1575-8725
More from this funder
Name:
National Institute for Health Research (NIHR)
Publisher:
Cell Press
Journal:
Cell Reports More from this journal
Volume:
41
Issue:
3
Article number:
111503
Publication date:
2022-10-18
Acceptance date:
2022-09-22
DOI:
ISSN:
2211-1247
Pmid:
36261000

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