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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 möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1535-6108
e-ISSN 1878-3686
Zeitschrift Cancer Cell
Quellenangaben Band: 5, Heft: 5, Seiten: 455-463 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOX)