Journal
ONCOGENE
Volume 34, Issue 2, Pages 135-143Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2013.605
Keywords
methionine; anti-folates; methylation; epigenetics; cancer therapy
Funding
- Ministerio de Ciencia e Innovacion (MICINN) [SAF2009-12043-C02-01]
- Fundacion Seneca (FS) [15230/PI/10]
- Fundacion de la Asociacion Espanola contra el Cancer (FAECC)
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Cancer is characterized 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 nonhistone 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 anticancer therapies. The application of these new epigenetic therapies could be of utility in the promotion of E2F1-dependent apoptosis in cancer cells, in avoiding metastatic pathways and/or in sensitizing tumour cells to radiotherapy.
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