期刊
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
卷 113, 期 -, 页码 47-56出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcdb.2020.09.001
关键词
CtIP; RBBP8; BRCA1; DNA end resection; double-strand break repair; replication stress; genome instability; pancreatic cancer; synthetic lethality; transcriptional regulation; tumour suppressor
资金
- Swiss National Science Foundation [31003A_176161]
- Swiss Cancer Research Foundation [KFS-4702-02-2019]
- Swiss National Science Foundation (SNF) [31003A_176161] Funding Source: Swiss National Science Foundation (SNF)
Human CtIP plays a crucial role in DNA repair, contributing to both genome integrity maintenance and oncogenic chromosomal translocations. Additionally, CtIP is involved in transcriptional regulation, DNA damage checkpoint signaling, and replication fork protection pathways.
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 doublestrand 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.
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