The Landscape of Histone Modification in Cancer Metastasis

Abstract

Metastasis represents one of the most devastating aspects of cancer. Epithelial to mesenchymal transition (EMT) has been shown to play a critical role in tumorigenic metastasis. During metastatic progression, both genetic and epigenetic modifications endow cancer cells with properties that modulate the capacity for metastatic success. Histone modification is profoundly altered in cancer cells and contributes to cancer metastasis by controlling different metastatic phenotypes. Here, we first review histone modifications and discuss their roles in EMT and metastasis, with a particular focus on histone methylation and acetylation. Second, we review the major histone modification enzymes that control chromatin in cancer metastasis. Third, we discuss the transcriptional regulation concerted by these enzymes with EMT transcription factors at different molecular layers. Finally, we discuss pharmacologic manipulation of histone modification enzymes for metastasis treatment. A comprehensive understanding of histone modification in metastasis will not only provide new insights into our knowledge of cancer progression and metastasis, but also offer a novel approach for the development of innovative therapeutic strategies.

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“…Increasing evidence suggests the role of epigenetic events in the development and/ or progression of gliomas [83]. Some genes are abnormally methylated in glioblastoma [84][85][86][87][88][89][90][91][93][94][95][96].…”

“…'Euchromatin' is an open chromatin structure that affords accessibility of transcription factors to DNA, resulting in gene activation. In contrast, 'heterochromatin' is a closed chromatin structure with a low interaction between transcription factors and the genome, leading to gene repression [94,95].…”