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Keywords = FAMCM

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8 pages, 581 KiB  
Review
Regulation of Replication Stress in Alternative Lengthening of Telomeres by Fanconi Anaemia Protein
by Duda Li, Kailong Hou, Ke Zhang and Shuting Jia
Genes 2022, 13(2), 180; https://doi.org/10.3390/genes13020180 - 20 Jan 2022
Cited by 5 | Viewed by 3594
Abstract
Fanconi anaemia (FA)-related proteins function in interstrand crosslink (ICL) repair pathways and multiple damage repair pathways. Recent studies have found that FA proteins are involved in the regulation of replication stress (RS) in alternative lengthening of telomeres (ALT). Since ALT cells often exhibit [...] Read more.
Fanconi anaemia (FA)-related proteins function in interstrand crosslink (ICL) repair pathways and multiple damage repair pathways. Recent studies have found that FA proteins are involved in the regulation of replication stress (RS) in alternative lengthening of telomeres (ALT). Since ALT cells often exhibit high-frequency ATRX mutations and high levels of telomeric secondary structure, high levels of DNA damage and replicative stress exist in ALT cells. Persistent replication stress is required to maintain the activity of ALT mechanistically, while excessive replication stress causes ALT cell death. FA proteins such as FANCD2 and FANCM are involved in the regulation of this balance by resolving or inhibiting the formation of telomere secondary structures to stabilize stalled replication forks and promote break-induced repair (BIR) to maintain the survival of ALT tumour cells. Therefore, we review the role of FA proteins in replication stress in ALT cells, providing a rationale and direction for the targeted treatment of ALT tumours. Full article
(This article belongs to the Section Molecular Genetics and Genomics)
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