ArticleAmerican journal of translational research2025
TS-1 inhibits endometrial cancer cell proliferation, migration, and apoptosis by blocking the PI3K/AKT/mTOR signaling pathway.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis.Translational oncology · 2026Article
- The therapeutic potential of botanicals: how medicinal plants targeting autophagy can reverse metabolic-associated fatty liver disease.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTS-1, an oral fluoropyrimidine-based antitumor agent, is widely used as a first-line therapy for various cancers. This study aimed to investigate the effects and underlying molecular mechanisms of TS-1 on endometrial cancer (EC) cell progression.
methodsHEC-1-A and Ishikawa EC cell lines were treated with different doses of TS-1 (0, 5, 10, 25, and 50 μg/mL). Cell viability, proliferation, migration, invasion, and apoptosis were assessed. The expression levels of Bcl-2-associated X protein (Bax; pro-apoptotic protein), B-cell lymphoma 2 (Bcl-2; anti-apoptotic protein), and key proteins in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway were analyzed. Furthermore, rescue experiments were performed using the PI3K activator 740 Y-P to determine whether TS-1 inhibits EC cell progression via the PI3K/AKT/mTOR pathway.
resultsTS-1 treatment markedly inhibited EC cell proliferation, migration, and invasion, while increasing apoptosis. The half-maximal inhibitory concentration (IC
conclusionTS-1 suppresses proliferation, migration, and invasion while promoting apoptosis in EC cells by suppressing the PI3K/AKT/mTOR signaling pathway. These data indicate that TS-1 may serve as a promising therapeutic agent for EC.
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Registered trials
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