ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
ANKRD1 expression and functional mechanism in stomach adenocarcinoma.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundANKRD1 is implicated in various cancers, but its role in stomach adenocarcinoma (STAD) remains unclear.
methodsANKRD1 expression and its prognostic value in STAD were analyzed using TIMER, UALCAN, GEPIA, and Kaplan-Meier plotter. Immune cell infiltration was evaluated via CIBERSORT and Single-sample Gene Set Enrichment Analysis (ssGSEA). Somatic mutations were analyzed from TCGA data. Functional enrichment analysis (GO, KEGG, GSEA (Gene Set Enrichment Analysis)) was performed on ANKRD1-associated genes. Subsequently, in vitro experiments were conducted. ANKRD1 protein levels were examined in STAD cell lines by Western blot. Stable knockdown and overexpression models were created. Functional assays (CCK-8, Transwell, and wound healing) assessed proliferation, migration, and invasion. Western blot measured STAT3 pathway activity.
resultsANKRD1 was significantly overexpressed in STAD tissues, and high expression correlated with poorer overall, first progression, and post-progression survival. ANKRD1 expression positively correlated with M0 macrophage and activated mast cell infiltration and negatively with resting memory CD4 + T cells and naive B cells. Although ANKRD1 itself was not mutated, associated genes were enriched in pathways like Wnt signaling. In vitro, ANKRD1 knockdown inhibited cell proliferation, migration, and invasion, while its overexpression promoted these effects. ANKRD1 was found to modulate STAT3 phosphorylation.
conclusionsANKRD1 is overexpressed in STAD and predicts poor prognosis. It promotes tumor cell proliferation, migration, and invasion, likely through activating the STAT3 signaling pathway, and correlates with an altered immune microenvironment.
Indexed as
Identifiers
41770518What 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.