ArticlePloS one2026
Effects of high CD93 expression on tumor growth and angiogenesis in gastric adenocarcinoma.
Article in PloS one, 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
backgroundGastric cancer remains a major cause of cancer-related mortality worldwide, with tumor recurrence and distant metastasis being primary contributors to poor prognosis; however, the underlying molecular mechanisms are not fully understood. CD93, a type I transmembrane glycoprotein, has been implicated in tumor angiogenesis and metastasis in various solid cancers, yet its role in gastric adenocarcinoma (STAD) requires further elucidation.
methodsWe analyzed CD93 expression and its prognostic significance in STAD using TCGA and an independent cohort. CD93 was overexpressed or knocked out in SGC-7901 cells, with modulation efficiency confirmed by qRT-PCR and Western blot. Functional assays included CCK-8, colony formation, tube formation, endothelial permeability, and transendothelial invasion. A xenograft model using Ctr and sg-CD93 cells was established to assess tumor growth, with IHC performed for Ki67, CD34, and α-SMA.
resultsCD93 was significantly upregulated in STAD tissues, and high expression correlated with poor patient survival. CD93 overexpression promoted cancer cell proliferation and enhanced tube formation in HUVECs. Interestingly, it also reduced endothelial monolayer permeability and inhibited transendothelial invasion of gastric cancer cells.
conclusionCD93 facilitates gastric adenocarcinoma progression by promoting tumor cell proliferation and angiogenesis. Its dual role in enhancing tube formation while reducing endothelial permeability suggests a complex mechanism in tumor microenvironment regulation, highlighting its potential as a therapeutic target.
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.