Human CtIP was originally identified as an interactor of the retinoblastoma protein and BRCA1, two bona fide tumour suppressors frequently mutated in cancer. CtIP is renowned for its role in the resection of DNA double-strand breaks (DSBs) during homologous recombination, a largely error-free DNA repair pathway crucial in maintaining genome integrity. However, CtIP-dependent DNA end resection is equally accountable for alternative end-joining, a mutagenic DSB repair mechanism implicated in oncogenic chromosomal translocations. In addition, CtIP contributes to transcriptional regulation of G1/S transition, DNA damage checkpoint signalling, and replication fork protection pathways. In this review, we present a perspective on the current state of knowledge regarding the tumour-suppressive and oncogenic properties of CtIP and provide an overview of their relevance for cancer development, progression, and therapy.

人类 CtIP 最初被确定为视网膜母细胞瘤蛋白和 BRCA1 的相互作用物，两个真正的肿瘤抑制因子在癌症中经常发生突变。CtIP 以其在同源重组过程中切除 DNA 双链断裂 (DSB) 中的作用而闻名，这是一种在很大程度上无错误的 DNA 修复途径，对于维持基因组完整性至关重要。然而，依赖 CtIP 的 DNA 末端切除同样负责替代末端连接，这是一种与致癌染色体易位有关的诱变 DSB 修复机制。此外，CtIP 有助于 G1/S 转换的转录调节、DNA 损伤检查点信号和复制叉保护途径。在这篇综述中，我们提出了关于 CtIP 的肿瘤抑制和致癌特性的当前知识状态的观点，并概述了它们与癌症发展、进展和治疗的相关性。