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Zhu, P.* ; Martin, E.* ; Mengwasser, J.* ; Schlag, P.* ; Janssen, K.-P.* ; Göttlicher, M.

Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis.

Cancer Cell 5, 455-463 (2004)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
Inappropriate transcriptional repression involving histone deacetylases (HDACs) is a prominent cause for the development of leukemia. We now identify faulty expression of a specific mediator of transcriptional repression in a solid tumor. Loss of the adenomatosis polyposis coli (APC) tumor suppressor induces HDAC2 expression depending on the Wnt pathway and c-Myc. Increased HDAC2 expression is found in the majority of human colon cancer explants, as well as in intestinal mucosa and polyps of APC-deficient mice. HDAC2 is required for, and sufficient on its own to prevent, apoptosis of colonic cancer cells. Interference with HDAC2 by valproic acid largely diminishes adenoma formation in APCmin mice. These findings point toward HDAC2 as a particularly relevant potential target in cancer therapy.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
ISSN (print) / ISBN 1535-6108
e-ISSN 1878-3686
Journal Cancer Cell
Quellenangaben Volume: 5, Issue: 5, Pages: 455-463 Article Number: , Supplement: ,
Publisher Cell Press
Publishing Place Cambridge, Mass.
Non-patent literature Publications
Reviewing status Peer reviewed