Publication: Targeting the epigenetic machinery of cancer cells
Authors
Fernández Pérez, María Piedad ; Sáez Ayala, Magalí ; Cabezas Herrera, Juan ; Montenegro Arce, María Fernanda ; Rodríguez López, José Neptuno ; Sánchez del Campo Ferrer, Luis
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Publisher
Springer Nature
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DOI
https://doi.org/10.1038/onc.2013.605
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info:eu-repo/semantics/article
Description
© 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
Abstract
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.
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Citation
Oncogene, 2015, Vol. 34, pp. 135–143
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