ArticleDiscover oncology2026
Ephrin-A4 ligand promotes gastric cancer cell epithelial-mesenchymal transition via the PI3K/AKT signaling pathway.
Article in Discover oncology, 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
Abstract
backgroundEphrin-A4 (EFNA4), a member of the ephrin ligand family, is known to be involved in the progression of various malignant neoplasms. Nonetheless, its specific functional implications in gastric cancer (GC) remain inadequately characterized. Therefore, this study aims to elucidate the underlying mechanisms by which EFNA4 influences GC. METHODS AND
resultsInitially, bioinformatics analyses revealed significantly elevated EFNA4 expression levels in gastric cancer tissues when compared with normal counterparts. Additionally, clinical assessments from a cohort of 93 GC patients demonstrated a correlation between EFNA4 expression and factors such as tumor size, AJCC stage, histological grade, and Ki-67 staining score. Furthermore, high levels of EFNA4 expression were associated with decreased overall survival, underscoring its potential as a prognostic biomarker. In vitro functional assays conducted in the human gastric cancer cell line AGS demonstrated that EFNA4 silencing markedly suppressed GC cell proliferation, invasion, and migration. Moreover, knockdown of EFNA4 impeded the process of epithelial-mesenchymal transition (EMT) through the modulation of the PI3K/AKT signaling pathway. Treatment with 740Y-P, a PI3K activator, was observed to enhance the expression of PI3K/AKT-related proteins and reverse the inhibition of malignant behavior in gastric cancer cells caused by EFNA4 knockdown.
conclusionsOur findings suggest that EFNA4 may act as an upstream regulator of the PI3K/AKT signaling pathway and could play a role in promoting EMT during the progression of gastric cancer.
Indexed as
Identifiers
What Socratic 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 Socratic graph.