Targeting the nucleic acid oxidative damage repair enzyme MTH1: a promising therapeutic option

Front Cell Dev Biol. 2024 Jan 31:12:1334417. doi: 10.3389/fcell.2024.1334417. eCollection 2024.

Abstract

The accumulation of reactive oxygen species (ROS) plays a pivotal role in the development of various diseases, including cancer. Elevated ROS levels cause oxidative stress, resulting in detrimental effects on organisms and enabling tumors to develop adaptive responses. Targeting these enhanced oxidative stress protection mechanisms could offer therapeutic benefits with high specificity, as normal cells exhibit lower dependency on these pathways. MTH1 (mutT homolog 1), a homolog of Escherichia coli's MutT, is crucial in this context. It sanitizes the nucleotide pool, preventing incorporation of oxidized nucleotides, thus safeguarding DNA integrity. This study explores MTH1's potential as a therapeutic target, particularly in cancer treatment, providing insights into its structure, function, and role in disease progression.

Keywords: DNA repair; MTH1; MTH1 inhibitor; therapeutic strategy; tumor.

Publication types

  • Review

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by grants from the National Natural Science Foundation of China (No. 82060505) and the Natural Science Foundation of Jiangxi Province (No. 20232BAB206106).