ArticleWorld journal of surgical oncology2026
Overexpression and prognostic value of aspartate β-hydroxylase in lung adenocarcinoma: a comprehensive study based on bioinformatics and clinical tissue sample validation.
Article in World journal of surgical 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.
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Abstract
backgroundLung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality worldwide. Although established biomarkers guide targeted therapy, their utility in prognostic stratification remains limited. In this study, we.
methodsASPH mRNA expression across pan-cancers and in LUAD was analyzed using the TIMER and The Cancer Genome Atlas (TCGA) databases. Immunohistochemical (IHC) staining was performed on 120 clinical LUAD specimens to validate ASPH protein expression. Kaplan-Meier survival analysis was used to assess the association between ASPH expression and overall survival (OS) as well as progression-free survival (PFS). Univariate and multivariate Cox proportional hazards regression models were applied to evaluate the prognostic value of ASPH. Gene Set Enrichment Analysis (GSEA) and Pearson co-expression analysis were conducted to explore potential molecular mechanisms.
resultsASPH was significantly upregulated in LUAD tissues at both mRNA and protein levels compared with corresponding normal lung tissues (all p < 0.001). High ASPH expression was closely correlated with aggressive clinicopathological features, including larger tumor size, T-stage parameters, lymph node/distant metastasis, and advanced clinical stage (all p < 0.05). Kaplan-Meier analysis showed that high ASPH expression was associated with poorer OS and PFS (both p < 0.001). Multivariate Cox regression confirmed ASPH as an independent prognostic factor for OS (TCGA cohort: HR = 1.01, 95% CI = 1.00–1.01, p = 0.003; clinical cohort: HR = 1.85, 95% CI = 1.03–3.30, p = 0.04) and PFS (clinical cohort: HR = 1.84, 95% CI = 1.08–3.14, p = 0.03). Co-expression analysis revealed ASPH was positively correlated with oncogenes RGS20 (r = 0.547) and MET (r = 0.516). GSEA indicated ASPH-coexpressed genes were enriched in pathways related to cell proliferation (ribosome, DNA replication, cell cycle), immune regulation (granulocyte activation, neutrophil-mediated immunity), and cell adhesion.
conclusionOverexpression of ASPH is significantly associated with poor prognosis and disease progression in LUAD patients, supporting its utility as a complementary prognostic tool and candidate therapeutic target for LUAD.
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