Posttranslational modifications to histone tails (histone marks) serve as the underlying basis for epigenetic signaling in the activation and repression of gene activity. The specific temporal and special context of these modifications is interpreted by nonhistone chromatin proteins called histone mark readers. The best-known example of reader proteins, heterochromatin protein 1 (HP1), recognizes epigenetic marks generated by histone methyltransferases (HMTs), SUV39H1 and G9a/GLP. Changes in the levels of HP1 and its associated HMTs have been associated with the development of several cancers. Here, we review the role of the HP1-HMT pathways in cancer-associated processes as well as the pharmacological targeting of this important epigenetic player for the therapy of malignant diseases.
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Velez et al. (2013) studied this question.
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