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Sci Signal2026;19(947):eadv4272.July 21, 2026Journal Article

NDRG1 expression in cancers confers dependence on DNA damage repair and sensitivity to quinacrine.

Garik V Mkrtchyan1, Alexander Veviorskiy2, Zarah G Meisen1, Michael A Petr1, Tobias Clausen Mercurio1, Daniela Bakula1, Peter Sykora3,4, Li-Wei Kuo4, Dean S Rosenthal4, Cynthia M Simbulan-Rosenthal4, Peiran Zhang5, Qiuqiong Tang5, Andreyan N Osipov6, Ivan V Ozerov1, Alex Aliper2, Alex Zhavoronkov2,7,8,9, Morten Scheibye-Knudsen1
1Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
2Insilico Medicine AI Limited, Abu Dhabi, UAE.
3Amelia Technologies LLC, Washington, DC 20001, USA.
4Department of Biochemistry and Molecular and Cellular Biology, Georgetown University School of Medicine, Washington, DC 20057, USA.
5Insilico Medicine Suzhou Ltd., Suzhou, China.
6CANDLE Synchrotron Research Institute, 31 Acharyan, 0040 Yerevan, Armenia.
7Insilico Medicine Hong Kong Limited, Hong Kong Science and Technology Park, Hong Kong, China.
8Insilico Medicine Canada Inc., 3710-1250 René-Lévesque Blvd. W, Montreal, Quebec H3B 4W8, Canada.
9Buck Institute for Research on Aging, Novato, CA 94945, USA.
PubMed DOI

Abstract

Cancer cells exploit DNA repair to overcome damage and errors induced by rapid proliferation and repressed checkpoints. Thus, the loss of one DNA repair protein can make tumors more susceptible to inhibition of other repair pathways. Here, using in silico methodologies and high-content genetic and cell survival screens, we found that the antimalarial drug quinacrine impaired the DNA damage respons…

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