Effects of high CD93 expression on tumor growth and angiogenesis in gastric adenocarcinoma

Gastric 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.

We 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.

CD93 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.

CD93 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.