The anti-cancer drugs curaxins target spatial genome organization

Omar L. Kantidze, Artem V. Luzhin, Ekaterina V. Nizovtseva, Alfiya Safina, Maria E. Valieva, Arkadiy K. Golov, Artem K. Velichko, Alexander V. Lyubitelev, Alexey V. Feofanov, Katerina V. Gurova (), Vasily M. Studitsky () and Sergey V. Razin ()
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Omar L. Kantidze: Institute of Gene Biology RAS
Artem V. Luzhin: Institute of Gene Biology RAS
Ekaterina V. Nizovtseva: Cancer Epigenetics Program, Fox Chase Cancer Center
Alfiya Safina: Roswell Park Comprehensive Cancer Center
Maria E. Valieva: Lomonosov Moscow State University
Arkadiy K. Golov: Institute of Gene Biology RAS
Artem K. Velichko: Institute of Gene Biology RAS
Alexander V. Lyubitelev: Lomonosov Moscow State University
Alexey V. Feofanov: Lomonosov Moscow State University
Katerina V. Gurova: Roswell Park Comprehensive Cancer Center
Vasily M. Studitsky: Cancer Epigenetics Program, Fox Chase Cancer Center
Sergey V. Razin: Institute of Gene Biology RAS

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract Recently we characterized a class of anti-cancer agents (curaxins) that disturbs DNA/histone interactions within nucleosomes. Here, using a combination of genomic and in vitro approaches, we demonstrate that curaxins strongly affect spatial genome organization and compromise enhancer-promoter communication, which is necessary for the expression of several oncogenes, including MYC. We further show that curaxins selectively inhibit enhancer-regulated transcription of chromatinized templates in cell-free conditions. Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. Thus, curaxins can be classified as epigenetic drugs that target the 3D genome organization.

Date: 2019
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DOI: 10.1038/s41467-019-09500-7

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