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Comment
. 2017 Nov 6;216(11):3429-3431.
doi: 10.1083/jcb.201710068. Epub 2017 Oct 24.

Cancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go!

Luisa Robbez-Masson  1 , Christopher H C Tie  1 , Helen M Rowe  2
Affiliations
Comment

Cancer cells, on your histone marks, get SETDB1, silence retrotransposons, and go!

Luisa Robbez-Masson et al. J Cell Biol. .

Abstract

Cancer cells thrive on genetic and epigenetic changes that confer a selective advantage but also need strategies to avoid immune recognition. In this issue, Cuellar et al. (2017. J. Cell Biol https://doi.org/10.1083/jcb.201612160) find that the histone methyltransferase SETDB1 enables acute myeloid leukemia cells to evade sensing of retrotransposons by innate immune receptors.

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Figures

Figure 1.
Figure 1.
SETDB1 enables AML cells to evade innate immune sensing of retrotransposons. Cancer cells elevate their levels of SETDB1, which promotes the formation of H3K9me3-based heterochromatin at retrotransposons. This in turn prevents transcription of retrotransposon-derived dsRNA and its downstream recognition by cytosolic RNA sensors. Genetic ablation of SETDB1 leads to a type I IFN response, the subsequent activation of ISGs, and apoptosis. LINE1, long interspersed nuclear element 1; sgRNA, single-guide RNA.
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