Por favor, use este identificador para citar o enlazar este ítem: https://doi.org/10.1038/onc.2013.605

Título: Targeting the epigenetic machinery of cancer cells
Fecha de publicación: 27-ene-2014
Editorial: Springer Nature
Cita bibliográfica: Oncogene, 2015, Vol. 34, pp. 135–143
ISSN: Print: 0950-9232
Electronic: 1476-5594
Palabras clave: Epigenetic
Cancer
Methylation
Antifolates
Non histone proteins
Resumen: Cancer is characterised by uncontrolled cell growth and the acquisition of metastatic properties. In most cases, the activation of oncogenes and/or deactivation of tumour suppressor genes lead to uncontrolled cell cycle progression and inactivation of apoptotic mechanisms. Although the underlying mechanisms of carcinogenesis remain unknown, increasing evidence links aberrant regulation of methylation to tumourigenesis. In addition to the methylation of DNA and histones, methylation of non-histone proteins, such as transcription factors, is also implicated in the biology and development of cancer. Because the metabolic cycling of methionine is a key pathway for many of these methylating reactions, strategies to target the epigenetic machinery of cancer cells could result in novel and efficient anti-cancer therapies. The application of these new epigenetic therapies could be of utility to promote E2F1-dependent apoptosis in cancer cells, avoid metastatic pathways and/or sensitise tumour cells to radiotherapy.
Autor/es principal/es: Montenegro Arce, María Fernanda
Sánchez del Campo Ferrer, Luis
Fernández Pérez, María Piedad
Sáez Ayala, Magalí
Cabezas Herrera, Juan
Rodríguez López, Jose Neptuno
Versión del editor: https://www.nature.com/articles/onc2013605#article-info
URI: http://hdl.handle.net/10201/147266
DOI: https://doi.org/10.1038/onc.2013.605
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 29
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Descripción: © 2014, The authors. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Accepted version of a Published Work that appeared in final form in Oncogene. To access the final edited and published work see https://doi.org/10.1038/onc.2013.605
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