SCR7, a potent cancer therapeutic agent and a biochemical inhibitor of nonhomologous DNA end‐joining

Abstract

Abstract Background DNA double‐strand breaks (DSBs) are harmful to the cell as it could lead to genomic instability and cell death when left unrepaired. Homologous recombination and nonhomologous end‐joining (NHEJ) are two major DSB repair pathways, responsible for ensuring genome integrity in mammals. There have been multiple efforts using small molecule inhibitors to target these DNA repair pathways in cancers. SCR7 is a very well‐studied anticancer molecule that blocks NHEJ by targeting one of the critical enzymes, Ligase IV. Recent findings In this review, we have highlighted the anticancer effects of SCR7 as a single agent and in combination with other chemotherapeutic agents and radiation. SCR7 blocked NHEJ effectively both in vitro and ex vivo. SCR7 has been used for biochemical studies like chromosomal territory resetting and in understanding the role of repair proteins in cell cycle phases. Various forms of SCR7 and its derivatives are discussed. SCR7 is also used as a potent biochemical inhibitor of NHEJ, which has found its application in improving genome editing using a CRISPR‐Cas system. Conclusion SCR7 is a potent NHEJ inhibitor with unique properties and wide applications as an anticancer agent. Most importantly, SCR7 has become a handy aid for improving genome editing across different model systems.

Keywords

• chemotherapy
• DNA double‐strand break
• DNA repair inhibitors
• genome editing
• homologous recombination
• nonhomologous DNA end‐joining