Studies on the Mechanism of Targeting Replication Stress Combined with Immune Checkpoint Inhibitors in Tumor Therapy
BAN Bingbing1,2, WEI Cheng1,3, WANG Cheng1,2*
RS (replication stress) refers to the slowing down, stopping or collapsing of DNA replication forks due to various factors, which will activate the cellular replication stress response to cope with the replication stress. However, if the replication stress exceeds the cell’s ability to repair itself, genomic instability or even cell death will be triggered. Drugs targeting RS kill tumor cells by this mechanism. Recently, it has been found that targeting RS can synergize with ICIs (immune checkpoint inhibitors) to enhance tumor killing, but the mechanism has not been fully elucidated. This review focuses on reviewing the research progress of combining targeted replicative stress with immune checkpoint inhibitors for the treatment of tumors to provide a theoretical basis for the development of more efficient tumor treatment strategies.
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