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. 2021 Dec 20;14:206. doi: 10.1186/s13045-021-01218-8

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Biological role of targeting DDR protein upon DNA damage in cancer cells. Upon DSB and replication stress, ATM, ATR, and DNA-PKcs are recruited to DNA damage sites, and ATM/CHK2 and ATR/CHK1 pathways are activated. In normal cells, ATM activates p53 by phosphorylation, leading to G1-phase arrest, senescence and apoptosis. However, in tumor cells, p53 is inactivated frequently, disrupting the G1-S cell cycle checkpoint, and making the cells dependent on G2-M cell cycle checkpoint for arrest upon DNA damage. The phosphorylation of WEE1 abolishes the activation of CDK1/2, inducing G2/M cell cycle arrest. PARP enzymes are primary proteins involved in SSB repair or base-excision repair (BER). Single-strand break (SSB); base excision repair (BER); double-strand breaks (DSB); non‐homologous end joining (NHEJ); homologous recombination (HR); ataxia telangiectasia mutated protein (ATM); poly-ADP-ribose polymerase (PARP); ataxia telangiectasia and Rad3-related protein (ATR); DNA-dependent protein kinase (DNA-PK); checkpoint kinase 1/2 (CHK1/2); cancer stem cells (CSCs); epithelial–mesenchymal transition (EMT)