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. 2022 Mar 28;60(5):54. doi: 10.3892/ijo.2022.5344

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Copyright: © Miyake et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Schema of the effect of adavosertib and ricolinostat on the G2/M checkpoint. In TP53-mutated cells, DNA repair is dependent on the G2/M checkpoint regulated by CDK1. CDK1 is a key regulator inducing cell cycle progression through the G2/M checkpoint. WEE1 phosphorylates and inhibits CDK1. Adavosertib inhibits WEE1 and then CDK1 is dephosphorylated and activated. Chk1 inhibits Cdc25, which dephosphorylates and activates CDK1. Ricolinostat decreases the phosphorylation of Chk1, indicating inhibition of Chk1. Chk, checkpoint kinase; ATR, ATR serine/threonine kinase; ATM, ATM serine/threonine kinase; CDK1, cyclin-dependent kinase 1; HDAC6, histone deacetylase 6; WEE1, WEE1 G2 checkpoint kinase.