Scholarlink

Background <p>Lung 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.</p> Methods <p>ASPH 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.</p> Results <p>ASPH was significantly upregulated in LUAD tissues at both mRNA and protein levels compared with corresponding normal lung tissues (all p &lt; 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 &lt; 0.05). Kaplan-Meier analysis showed that high ASPH expression was associated with poorer OS and PFS (both p &lt; 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.</p> Conclusion <p>Overexpression 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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Overexpression and prognostic value of aspartate β-hydroxylase in lung adenocarcinoma: a comprehensive study based on bioinformatics and clinical tissue sample validation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月31日

查看全文
  • Qingzhu Zheng,
  • Jiamiao Weng,
  • Bin Zhu,
  • Mingjie Li,
  • Xianjin Zhu,
  • Yingping Cao

摘要

Background

Lung 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.

Methods

ASPH 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.

Results

ASPH 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.

Conclusion

Overexpression 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.