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EPIGENETICS

Get to know your epigenetic target

Nature Reviews Cancer volume 19, pages 62–63 (2019)Cite this article

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Many epigenetic modifiers are activated in tumours and as such are considered potential therapeutic targets. Two studies now suggest caution is warranted in attempts to inhibit the histone methyltransferase G9a, as its loss can promote tumour development and evolution.

In line with previous results, non-tumour cells from G9acKO mice had reduced levels of histone H3 lysine 9 dimethylation (H3K9me2) and increased chromatin accessibility. The authors hypothesized that this chromatin profile might contribute to the development of late-onset SCCs by changing mutational profiles. The number and type (predominantly A > T transversions) of single nucleotide variants were largely similar between wild-type and G9acKO SCCs, with subtle differences that suggested a defect in nucleotide excision repair. However, G9acKO SCCs were more genomically unstable, with increased focal copy number gains.

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References

Original articles

  • Avgustinova, A. et al. Loss of G9a preserves mutation patterns but increases chromatin accessibility, genomic instability and aggressiveness in skin tumours. Nat. Cell Biol. 20, 1400–1409 (2018)

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  • Rowbotham, S. P. et al. H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression. Nat. Commun. 9, 4559 (2018)

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  1. Nature Reviews Cancer http://www.nature.com/nrc/

    Sarah Seton-Rogers

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  1. Sarah Seton-Rogers
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Correspondence to Sarah Seton-Rogers.

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Seton-Rogers, S. Get to know your epigenetic target. Nat Rev Cancer 19, 62–63 (2019). https://doi.org/10.1038/s41568-018-0103-7

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