Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability

Nayak Sumeet; Calvo Jennifer A.; Cantor Sharon B.

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Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability

机译：Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability

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Introduction: Translesion synthesis (TLS) is a DNA damage tolerance (DDT) mechanism that employs error-prone polymerases to bypass replication blocking DNA lesions, contributing to a gain in mutagenesis and chemo-resistance. However, recent findings illustrate an emerging role for TLS in replication gap suppression (RGS), distinct from its role in post-replication gap filling. Here, TLS protects cells from replication stress (RS)-induced toxic single-stranded DNA (ssDNA) gaps that accumulate in the wake of active replication. Intriguingly, TLS-mediated RGS is specifically observed in several cancer cell lines and contributes to their survival. Thus, targeting TLS has the potential to uniquely eradicate tumors without harming non-cancer tissues.

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来源
《Expert opinion on therapeutic targets》 |2021年第6期|27-36|共10页
作者
Nayak Sumeet; Calvo Jennifer A.; Cantor Sharon B.;
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作者单位

Univ Massachusetts, Med Sch, Dept Mol Cell & Canc Biol, 364 Plantat St,LRB 415, Worcester, MA 01605;

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原文格式 PDF
正文语种英语
中图分类药学;
关键词
Translesion synthesis (TLS); oncogene-induced replication stress; ssDNA gaps; replication gap suppression (RGS); replication stress response (RSR); DNA lesion bypass; mutagenesis; cancer and cancer therapeutics;

Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability

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