ArticleJournal of translational medicine2026
The small molecule compound ETP-46321 suppresses gastric cancer progression by inducing SAT1-mediated ferroptosis and inhibiting the PI3K/AKT/mTOR pathway.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Dual regulation of inflammation and ferroptosis: An injectable hydrogel targeting macrophages for the treatment of temporomandibular joint osteoarthritis and knee osteoarthritis.Materials today. Bio · 2026Article
- Naringenin, a Food-Derived Flavanone, Suppresses ITGA11-Associated Gastric Cancer Progression via the FAK/PI3K/AKT/mTOR Axis.Cancers · 2026Article
- Elucidating the dual regulation of apoptosis and migration by Ajugasterone C in AGS cells via the PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundGastric cancer (GC) remains a common malignant tumor of the digestive system, with persistently high incidence and mortality rates. Therefore, new and effective therapeutic strategies are urgently needed to improve its treatment.
methodsWe investigated the anti-GC effect and underlying mechanism of the small molecule compound ETP-46321. In vitro functional assays were performed to evaluate the effects of ETP-46321 on GC cell proliferation, migration, and apoptosis. RNA sequencing was employed to elucidate the potential molecular mechanism of ETP-46321 treatment. SAT1 knockdown was used to investigate its impact on the effect of ETP-46321 in GC cells, and overexpression of SAT1 was also utilized. Bioinformatics analysis was used to explore the related signaling pathways. IGF-1 intervention was used as a rescue experiment to explore the role of the PI3K/AKT signaling pathway in the anti-tumor effect of ETP-46321. Finally, organoid and nude mouse xenograft models were used to verify the anti-GC activity of ETP-46321.
resultsETP-46321 significantly inhibited the proliferation and migration of GC cells and induced cell apoptosis. Mechanistically, ETP-46321 could induce ferroptosis by upregulating SAT1. Knockdown of SAT1 reversed ETP-46321-mediated ferroptosis and restored cell proliferation and migration. Furthermore, ETP-46321 effectively inhibited the activity of the PI3K/AKT/mTOR signaling pathway, and this anti-cancer effect could be partially reversed by IGF-1, an activator of the PI3K/AKT/mTOR pathway. Both organoid and nude mouse xenograft models revealed the significant anti-GC activity of ETP-46321.
conclusionsThis study reveals a dual mechanism by which ETP-46321 exerts anti-GC effects by promoting SAT1-mediated ferroptosis and inhibiting the PI3K/AKT/mTOR signaling pathway. These findings provide important experimental evidence and theoretical support for the development of targeted GC therapies based on the mechanism of action of ETP-46321.
Indexed as
Identifiers
What OpenQuestion holds
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.