| Literature DB >> 26208904 |
Laia Simó-Riudalbas1, Montserrat Pérez-Salvia1, Fernando Setien1, Alberto Villanueva2, Catia Moutinho1, Anna Martínez-Cardús1, Sebastian Moran1, Maria Berdasco1, Antonio Gomez1, Enrique Vidal1, Marta Soler1, Holger Heyn1, Alejandro Vaquero3, Carolina de la Torre4, Silvia Barceló-Batllori4, August Vidal5, Luca Roz6, Ugo Pastorino7, Katalin Szakszon8, Guntram Borck9, Conceição S Moura10, Fátima Carneiro11, Ilse Zondervan12, Suvi Savola12, Reika Iwakawa13, Takashi Kohno13, Jun Yokota14, Manel Esteller15.
Abstract
Recent efforts to sequence human cancer genomes have highlighted that point mutations in genes involved in the epigenetic setting occur in tumor cells. Small cell lung cancer (SCLC) is an aggressive tumor with poor prognosis, where little is known about the genetic events related to its development. Herein, we have identified the presence of homozygous deletions of the candidate histone acetyltransferase KAT6B, and the loss of the corresponding transcript, in SCLC cell lines and primary tumors. Furthermore, we show, in vitro and in vivo, that the depletion of KAT6B expression enhances cancer growth, while its restoration induces tumor suppressor-like features. Most importantly, we demonstrate that KAT6B exerts its tumor-inhibitory role through a newly defined type of histone H3 Lys23 acetyltransferase activity. ©2015 American Association for Cancer Research.Entities:
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Year: 2015 PMID： 26208904 DOI： 10.1158/0008-5472.CAN-14-3702
Source DB: PubMed Journal: Cancer Res ISSN： 0008-5472 Impact factor: 12.701