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

作者信息

Ding Yifeng, Liu Qingquan

机构信息

Department of Hepatobiliary Surgery, The First Affiliated Hospital of Gannan Medical University, Jiangxi, China.

出版信息

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


DOI:10.3389/fcell.2024.1334417
PMID:38357002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10864502/
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 '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.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/c02b09863875/fcell-12-1334417-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/b5e826d547c3/fcell-12-1334417-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/607cb4209213/fcell-12-1334417-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/c02b09863875/fcell-12-1334417-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/b5e826d547c3/fcell-12-1334417-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/607cb4209213/fcell-12-1334417-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb5/10864502/c02b09863875/fcell-12-1334417-g003.jpg

相似文献

[1]
Targeting the nucleic acid oxidative damage repair enzyme MTH1: a promising therapeutic option.

Front Cell Dev Biol. 2024-1-31

[2]
Role of MTH1 in oxidative stress and therapeutic targeting of cancer.

Redox Biol. 2024-11

[3]
Mechanisms of MTH1 inhibition-induced DNA strand breaks: The slippery slope from the oxidized nucleotide pool to genotoxic damage.

DNA Repair (Amst). 2019-3-2

[4]
Targeting human MutT homolog 1 (MTH1) for cancer eradication: current progress and perspectives.

Acta Pharm Sin B. 2020-12

[5]
MTH1 as a Chemotherapeutic Target: The Elephant in the Room.

Cancers (Basel). 2017-5-8

[6]
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Colloids Surf B Biointerfaces. 2022-10

[7]
MutT Homolog 1 (MTH1) maintains multiple KRAS-driven pro-malignant pathways.

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[8]
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[9]
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Nat Commun. 2023-8-10

[10]
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Lung Cancer. 2017-7

引用本文的文献

[1]
The identification and prediction of lung adenocarcinoma prognosis using a novel gene signature associated with DNA replication.

Transl Cancer Res. 2025-3-30

[2]
Role of MTH1 in oxidative stress and therapeutic targeting of cancer.

Redox Biol. 2024-11

本文引用的文献

[1]
Integration of Activation by Hypoxia and Inhibition Resistance of Tumor Cells to Apoptosis for Precise and Augmented Photodynamic Therapy.

Adv Healthc Mater. 2023-10

[2]
Light-Elicited and Oxygen-Saved Iridium Nanocapsule for Oxidative Damage Intensified Oncotherapy.

Molecules. 2023-5-28

[3]
Advances in immunotherapy for glioblastoma multiforme.

Front Immunol. 2022

[4]
miR-4478 Accelerates Nucleus Pulposus Cells Apoptosis Induced by Oxidative Stress by Targeting MTH1.

Spine (Phila Pa 1976). 2023-3-1

[5]
Platinum-based nanocomposites loaded with MTH1 inhibitor amplify oxidative damage for cancer therapy.

Colloids Surf B Biointerfaces. 2022-10

[6]
Targeting the DNA repair enzymes MTH1 and OGG1 as a novel approach to treat inflammatory diseases.

Basic Clin Pharmacol Toxicol. 2022-8

[7]
Redox signaling at the crossroads of human health and disease.

MedComm (2020). 2022-3-31

[8]
8-oxoguanine and 8-oxodeoxyguanosine Biomarkers of Oxidative DNA Damage: A Review on HPLC-ECD Determination.

Molecules. 2022-3-1

[9]
Inhibition of Oxidized Nucleotide Sanitation By TH1579 and Conventional Chemotherapy Cooperatively Enhance Oxidative DNA Damage and Survival in AML.

Mol Cancer Ther. 2022-5-4

[10]
Real-world PM exposure induces pathological injury and DNA damage associated with miRNAs and DNA methylation alteration in rat lungs.

Environ Sci Pollut Res Int. 2022-4

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