ReviewRedox biology2024
Role of MTH1 in oxidative stress and therapeutic targeting of cancer.
Review in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- One-pot synthesis of Mn/Fe bimetal-doped metal-organic framework as multifunctional nanocarriers for esophageal cancer targeted therapy.Journal of pharmaceutical analysis · 2026Article
- CEMs-SELEX: DNAzyme-powered de novo biomarker discovery and noninvasive cancer diagnosis.Science advances · 2026Article
- NUDT1 drives osteosarcoma progression and serves as a robust predictor of clinical outcomes.Cancer cell international · 2026Article
- Amikacin-eravacycline combination mediates the synergistic elimination of carbapenem-resistant pathogens via in vitro and in vivo metabolic reprogramming.PLoS pathogens · 2026Article
- Sequential release of MTH1 inhibitor and chemotherapeutic drug using a pH-sensitive polymeric delivery system induces apoptosis in human tongue squamous cell carcinoma CAL-27 cells in vitro.World journal of surgical oncology · 2025Article
- Repurposing resveratrol for redox-mediated inhibition of MTH1 in breast cancer.Scientific reports · 2025Article
- Observational
- Photodynamic Therapy and Dietary Antioxidants: A Dual Strategy for Genome Stability and DNA Damage Repair.Cancer medicine · 2025Review
- Antioxidants in cancer therapy mitigating lipid peroxidation without compromising treatment through nanotechnology.Discover nano · 2025Review
- The identification and prediction of lung adenocarcinoma prognosis using a novel gene signature associated with DNA replication.Translational cancer research · 2025Article
- Article
- Phytochemical composition, in vitro cytotoxicity and in silico ADME/Tox analysis of the active compounds of3 Biotech · 2025Article
- Oxidative stress-related genes in uveal melanoma: the role of CALM1 in modulating oxidative stress and apoptosis and its prognostic significance.Frontiers in oncology · 2025Article
- Emodin-induced cell cycle arrest: A promising approach for cancer therapy (Review).Medicine internationalReview
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells maintain high levels of reactive oxygen species (ROS) to drive their growth, but ROS can trigger cell death through oxidative stress and DNA damage. To survive enhanced ROS levels, cancer cells activate their antioxidant defenses. One such defense is MTH1, an enzyme that prevents the incorporation of oxidized nucleotides into DNA, thus preventing DNA damage and allowing cancer to proliferate. MTH1 levels are often elevated in many cancers, and thus, inhibiting MTH1 is an attractive strategy for suppressing tumor growth and metastasis. Targeted MTH1 inhibition can induce DNA damage in cancer cells, exploiting their vulnerability to oxidative stress and selectively targeting them for destruction. Targeting MTH1 is promising for cancer treatment because normal cells have lower ROS levels and are less dependent on these pathways, making the approach both effective and specific to cancer. This review aims to investigate the potential of MTH1 as a therapeutic target, especially in cancer treatment, offering detailed insights into its structure, function, and role in disease progression. We also discussed various MTH1 inhibitors that have been developed to selectively induce oxidative damage in cancer cells, though their effectiveness varies. In addition, this review provide deeper mechanistic insights into the role of MTH1 in cancer prevention and oxidative stress management in various diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.