ArticleCancer research and treatment2025
Identifying Anti-cancer Effects and Exploring the Mechanism of an MPS1/TTK Inhibitor in Gastric Cancer.
Article in Cancer research and treatment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed.
- Molecular and Phenotypic Characterization of Fluid-Derived Patient-Derived Cell and Organoid Models in Advanced Gastric Cancer.Journal of gastric cancer · 2026Article
- Analytical and clinical validation of CancerMaster, an automated targeted NGS panel, for tumor-only precision oncology.Scientific reports · 2026Article
- Article
- ETS Family Transcription Factors in Gastric Cancer and the Role of ELF3 in the Core Metaplasia Transcription Factor Network.Oncology research · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
purposeThis study aimed to identify the anti-cancer effect and investigate the underlying mechanism of MPS1/TTK (monopolar spindle 1; also known as threonine tyrosine kinase) inhibitor in gastric cancer (GC) cell lines. Materials and Methods: This study used compound-9, a highly selective MPS1/TTK inhibitor, to evaluate its anti-cancer effects on GC cell lines. Cell viability assay was performed to determine sensitivity to the inhibitor. Cell cycle analysis and apoptosis assays were performed using Flow cytometry to evaluate the effects of the inhibitor. Protein-expression levels were analyzed through western blotting after the inhibitor treatment.
resultsThe Epstein-Barr virus and microsatellite-instable-high groups tended to be sensitive to the inhibitor, while the genomically stable (GS)-likely group tended to be moderate-to-resistant. In contrast, the chromosomal instability (CIN)-likely group was extremely sensitive or resistant. Within the CIN group, TP53WT cell lines were sensitive, whereas TP53MUT cell lines were sensitive or resistant. Upon treatment of the inhibitor, the TP53WT-sensitive cell line underwent cell death more rapidly compared to the TP53MUT-sensitive cell line. In contrast, the TP53MUT-sensitive cell experienced higher levels of aneuploidy or polyploidy and underwent cell death at later time point than the TP53WT-sensitive cell line. The TP53MUT-resistant line can tolerate aneuploidy or polyploidy and exhibits drug resistance.
conclusionOur study explores the potential of an MPS1/TTK inhibitor, compound-9, as a targeted therapy in GC cells and investigates its mechanism of action.
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