ArticleCancer chemotherapy and pharmacology2026
Homoharringtonine suppresses gastric cancer progression by targeting PI3K/ AKT/FOXO pathway and impairing the GSH-GPX4 antioxidant axis.
Article in Cancer chemotherapy and pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the unexplored therapeutic potential and identify the specific molecular targets of homoharringtonine (HHT) in gastric cancer (GC).
methodsHHT’s efficacy was evaluated in GC cell lines (MKN1/MKN45), normal epithelial cells (GES-1), and an HGC27 xenograft model. Mechanisms were investigated using RNA-sequencing, microscale thermophoresis (MST), molecular docking, and biochemical assays.
resultsHHT suppressed GC cell proliferation and migration, inducing G1-phase arrest and apoptosis, while demonstrating lower cytotoxicity toward normal GES-1 cells. MST and docking assays confirmed that HHT directly and stably binds to AKT (KD= 6.496 nM) and suppresses the PI3K/AKT/FOXO/GSK3β signaling pathway. Concurrently, transcriptomic profiling and experimental validation showed that HHT disrupts glutathione metabolism. It depleted intracellular GSH and downregulated GPX4, triggering ferroptosis-like oxidative damage and mitochondrial cristae loss. In vivo, HHT inhibited GC xenograft tumor growth without causing systemic toxicity, which was accompanied by decreased Ki-67 and increased Caspase-3 expression.
conclusionHHT inhibits GC progression by suppressing AKT-mediated tumor growth and inducing GPX4-dependent ferroptosis. These findings highlight HHT as a promising targeted therapeutic for GC.
Indexed as
Identifiers
42050199What 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.