ArticleOncology letters2021
Antitumour activity of TH1579, a novel MTH1 inhibitor, against castration-resistant prostate cancer.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- The MTH1 inhibitor TH287 sensitized Castration-Resistant Prostate Cancer cells to ionizing radiation therapy.International urology and nephrology · 2026Article
- Targeting the nucleic acid oxidative damage repair enzyme MTH1: a promising therapeutic option.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Castration-resistant prostate cancer (CRPC) treatment still remains difficult. The aim of the present study was to determine the antitumour efficacy of the MutT homolog 1 (MTH1) inhibitor, TH1579, against castration-resistant prostate cancer. PC-3 and DU-145 prostate cancer cells were treated with different concentrations of TH1579. C4-2 cells with or without androgen receptor (AR) were also treated with TH1579 to assess AR function. Cell survival, 8-oxo-dG levels and DNA damage were measured using cell viability assays, western blotting, immunofluorescence analysis and flow cytometry. TH1579 inhibited CRPC cell proliferation in a dose-dependent manner. The viabilities of PC-3 and DU-145 cells treated with 1 µM of TH1579 were 28.6 and 24.1%, respectively. The viabilities of C4-2 cells with and without AR treated with 1 µM TH1579 were 10.6 and 19.0%, respectively. Moreover, TH1579 treatment increased 8-oxo-dG levels, as well as the number of 53BP1 and γH2A.X foci, resulting in increased DNA double-strand breakage and apoptosis in PC-3 and DU-145 cells. The findings of the present study demonstrated that TH1579 exerted strong antitumour effects on CRPC cells, and may therefore be used as a potential therapeutic agent for the clinical treatment of CRPC.
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Registered trials
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