ArticleBMC cancer2025
ASPN was higher expression in gastric cancer and associated with poor prognosis through promoting invasion and migration and inducing macrophage M2 polarization.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Exploration and experimental verification of triaptosis-related prognostic genes and cells in gastric cancer.Molecular biology reports · 2026Article
- Screening of molecular biomarkers ASPN and LBH and construction of a prediction nomogram for the progression of esophagogastric junction adenocarcinoma.Journal of gastrointestinal oncology · 2026Article
- Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.Biomarker research · 2026Review
- Multi-omics investigation of benzo[a]pyrene in gastric cancer: comprehensive network toxicology, machine learning and molecular docking approaches.Molecular diversity · 2026Article
- ANP32A interacts with LDHA to modulate glycolysis and ferroptosis in hepatocellular carcinoma.Frontiers in oncology · 2026Article
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4 authors.
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Abstract
aimAsporin (ASPN) was shown to be highly expressed in gastric cancer. The purpose of this study was to investigate the relationship between ASPN expression and invasion, migration, macrophage M2 polarization and prognosis of gastric cancer.
methodsASPN expression in tumor and normal tissues was analyzed using TIMER, GEPIA, and HPA databases. Its clinical prognostic value was evaluated using Kaplan-Meier plotter and GEPIA databases. The association of ASPN with clinicopathological parameters was explored using the cBioPortal datasets. The TIMER and Aclbi databases were used to assess the relationship between ASPN and tumor immune infiltration, and TIMER and GEPIA were used to analyze correlations with immune infiltrate gene markers. Immunohistochemistry detected ASPN protein in 436 gastric cancer tissues and analyzed its correlation with clinicopathological parameters and prognosis. Transwell assays were used to assess ASPN's impact of ASPNs on the migration and invasion of HGC27 and AGS gastric cancer cells. GSEA was used to investigate cellular mechanisms associated with ASPN expression. The possible regulatory pathways of ASPN that promote M2 macrophage polarization were analyzed using RNA-seq.
resultsASPN expression was elevated in 51.8% of gastric cancer cases and was correlated with poor survival rates, higher tumor stage, and histologic grade. It is significantly linked to the presence of various immune cells and markers, particularly monocytes/macrophages and regulatory T (Treg) cells. High ASPN expression is associated with multiple cancer-related pathways. ASPN upregulation is linked to the Lauren classification, differentiation, invasion depth, lymph node and distant metastasis, and TNM staging. Patients with low ASPN expression had a 5-year survival rate of 53.8% compared to 28.8% for those with high expression. Overexpression of ASPN upregulates migration and invasion of AGS and HGC-27 cells. TIMER database analysis indicated that ASPN was positively correlated with M2 macrophage markers (such as CD163) but not with M1 markers. ASPN upregulation in gastric cancer is closely associated with M2 macrophage polarization and a poor prognosis. KEGG pathway analysis revealed that increased ASPN levels are significantly associated with the neutrophil extracellular trap (NETs) pathway.
conclusionsASPN is highly expressed in gastric cancer and is associated with poor prognosis by promoting invasion and migration and inducing macrophage M2 polarization.
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