武汉大学人民医院检验医学中心 湖北 武汉 430060
霍晓丽,女,2001—,医学硕士生,主要从事肝癌生物标志物研究,E⁃mail:2024283020216@whu.edu.cn。
包安裕,E⁃mail:bay@whu.edu.cn。
收稿:2025-06-13,
纸质出版:2026-10-25
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霍晓丽,袁梦馨,陈新宇等.ASPM基因在肝细胞癌中的表达分析及其预后价值[J].武汉大学学报(医学版),2026,47(10):1382-1390.
HUO Xiaoli,YUAN Mengxin,CHEN Xinyu,et al.Expression analysis and prognostic value of ASPM gene in hepatocellular carcinoma[J].Medical Journal of Wuhan University,2026,47(10):1382-1390.
霍晓丽,袁梦馨,陈新宇等.ASPM基因在肝细胞癌中的表达分析及其预后价值[J].武汉大学学报(医学版),2026,47(10):1382-1390. DOI: 10.14188/j.1671-8852.2025.0609.
HUO Xiaoli,YUAN Mengxin,CHEN Xinyu,et al.Expression analysis and prognostic value of ASPM gene in hepatocellular carcinoma[J].Medical Journal of Wuhan University,2026,47(10):1382-1390. DOI: 10.14188/j.1671-8852.2025.0609.
目的
2
纺锤体微管组装因子(ASPM)基因与多种肿瘤的预后相关,该研究旨在通过生物信息学方法分析ASPM基因在肝细胞癌中的表达特点及其预后价值。
方法
2
在GEO数据库中获取肝细胞癌相关基因表达谱,并利用eVITTA数据库分析肝细胞癌与非肿瘤肝组织之间的差异表达基因(DEGs);利用GEPIA、UALCAN和TNMplot数据库对ASPM基因进行表达分析;利用Kaplan Meier‑Plotter数据库对ASPM基因进行生存分析;基于STRING数据库和Cytoscape软件构建蛋白质⁃蛋白质相互作用(PPI)网络;利用GO和KEGG数据库对DEGs进行生物学功能分析;利用muTarget数据库分析影响ASPM基因表达的突变基因。
结果
2
与非肿瘤肝组织相比,ASPM基因在肝细胞癌中显著上调(
P
<
0.05),且其高表达时,肝细胞癌患者生存率显著下降(
P
<
0.05)。使用GEPIA、UALCAN、TNMplot和muTarget数据库发现,ASPM基因表达水平受多种临床病理因素及基因突变的影响,其中TP53和CTNNB1的突变率最高,TP53突变导致ASPM基因高表达,CTNNB1突变导致ASPM基因低表达(
P
<
0.01)。PPI网络发现,ASPM基因作为关键基因与其他基因存在密切联系。上调差异表达基因显著富集在核染色体分离和核分裂等生物过程,下调差异表达基因主要参与内吞作用的正向调节等生物过程。
结论
2
ASPM基因在肝细胞癌患者中过度表达,并与肝细胞癌患者不良预后密切相关,可能成为肝细胞癌预后及监测的潜在生物标志物。
Objective
2
To systematically characterize the expression of the assembly factor for spindle microtubules (ASPM) gene and evaluate its prognostic significance in hepatocellular carcinoma (HCC) using bioinformatics approaches.
Methods
2
Gene expression profiles of HCC were downloaded from the GEO database
and differentially expressed genes (DEGs) between tumor and non⁃tumor liver tissues were identified using eVITTA. ASPM expression was validated using GEPIA
UALCAN
and TNMplot. Survival analysis was performed using Kaplan⁃Meier Plotter. A protein⁃protein interaction (PPI) network was constructed using STRING and visualized with Cytoscape. DEGs were functionally annotated using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Mutated genes potentially influencing ASPM expression were surveyed using muTarget.
Results
2
Compared with adjacent non⁃tumor liver tissues
ASPM expression was significantly up⁃regulated in HCC (
P
<
0.05)
and high ASPM levels were associated with shorter overall survival (
P
<
0.05). Integrated analysis using GEPIA
UALCAN
TNMplot
and muTarget indicated that ASPM expression correlated with multiple clinicopathological parameters and somatic mutations. TP53 and CTNNB1 exhibited the highest mutation frequencies; TP53 mutations were associated with elevated ASPM expression
whereas CTNNB1 mutations correlated with reduced expression (both
P
<
0.01). In the PPI network
ASPM ranked as a hub gene tightly connected with cell⁃cycle regulators. Up⁃regulated DEGs were enriched in mitotic nuclear division and chromosome segregation
while down⁃regulated DEGs were mainly involved in positive regulation of endocytosis.
Conclusion
2
The ASPM gene is overexpressed in HCC and closely associated with poor prognosis
indicating its potential as a biomarker for prognosis and disease monitoring.
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