ArticleBiology direct2026
DLAT inhibits ferroptosis to promote malignant progression of gastric cancer through Nrf2/HO-1/GPX4 signaling pathway.
Article in Biology direct, 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
4 authors.
Funding
Abstract
backgroundFerroptosis is a novel regulatory mechanism of cell death caused by iron-dependent lipid peroxidation (lipid-ROS) accumulation. The aim of this study was to explore whether dihydrolipoic acid transacetylase (DLAT) influences ferroptosis to promote the progression of gastric cancer (GC).
methodsThe expression of DLAT in GC tissues and cell lines was examined by qRT-PCR, western blotting, and immunohistochemistry. Kaplan–Meier survival curve analysis was used to estimate overall survival, and the log-rank test was used to estimate recurrence-free survival. The functional role of DLAT in GC was evaluated using in vitro and in vivo experiments including MTT, scratch healing tests, transwell assays and a xenograft tumor mouse model. Ferroptosis was evaluated by using malondialdehyde (MDA), reduced glutathione (GSH), lactate dehydrogenase (LDH), and superoxide dismutase (SOD) detection kits, iron accumulation assays, lipid ROS quantification, and mitochondrial deep red fluorescence staining kits. Western blotting was used to detect the biomarkers of ferroptosis and the interactions between DLAT and Nrf2, HO-1 and GPX4.
resultsWe found that DLAT was upregulated in GC cells and tissues, and high DLAT expression indicated poor prognosis. Knockdown of DLAT inhibited the proliferation, invasion and metastasis of GC cells by increasing the levels of MDA and LDH, promoting the accumulation of Fe2+ and lipid ROS, consuming GSH and SOD, reducing mitochondrial membrane potential, and suppressing the expression of GPX4. Overexpression of GPX4 can specifically salvage the growth inhibition of GC cells caused by DLAT knockdown, but did not affect the activity of the upstream DLAT, Nrf2 and HO-1. The inhibition of ferroptosis by DLAT was related to the regulation of the Nrf2/HO-1/GPX4 antioxidant axis. In vivo, DLAT inhibited the Nrf2/HO-1 axis, hindering the growth of transplanted tumors.
conclusionThese results indicated that DLAT deficiency increased accumulation of Fe2+ and lipid ROS, enhanced disruption of mitochondrial membrane potential, and induced ferroptosis through the Nrf2/HO-1/GPX4 axis, thereby inhibiting the malignant progression of GC cells. DLAT serves as a prognostic biomarker and potential therapeutic target for GC.
trial registrationRegistry and the Registration of the study/trial: N/A.
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.