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AURKB as a key driver of esophageal cancer progression: Molecular mechanisms and potential nursing implications based
Xiaoling Qu1, Lihua Lu2, Xuan Dong3
1Gastrointestinal Rehabilitation Center, Beijing Rehabilitation Hospital Affiliated to Capital Medical University, Shijingshan District, Beijing, China.
Abstract:
Esophageal cancer is a highly heterogeneous malignant tumor with a high global incidence and poor prognosis. Its molecular mechanisms are complex and have not yet been fully clarified. The protein kinase encoded by AURKB plays a key role in cell cycle regulation and mitosis; however, its expression characteristics, functional mechanisms, nursing care in esophageal cancer have not yet been clarified, thus urgently require in-depth research. This study integrates bioinformatics analysis and validation with public datasets. Based on GSE164158 and GSE17351 datasets from gene expression omnibus database, differentially expressed genes (DEGs) between esophageal cancer and normal tissues were screened. Functional enrichment analysis was performed using GO, KEGG, GSEA, Metascape to analyze biological pathways involved in DEGs. Protein-protein interaction networks were constructed using STRING database and Cytoscape, core modules were identified by combining MCODE algorithm. Key gene modules related to esophageal cancer phenotypes were screened through weighted gene co-expression network analysis, core genes were further screened by integrating DEGs results. Core genes were identified using multiple algorithms (CLUSTER ONE and MCC), immune infiltration characteristics were analyzed via CIBERSORT. A total of 1500 DEGs were screened out, which were significantly enriched in biological processes and pathways such as cell cycle, DNA replication, mitosis. Metascape analysis further verified that DEGs are involved in key processes including cell cycle regulation and DNA repair. Integrated analysis of the PPI network and weighted gene co-expression network analysis showed that three hundred forty nine genes were present in both key modules and DEGs; combined with screening via multiple algorithms, 4 core genes were finally identified. AURKB was highly expressed in esophageal cancer tissues (validated by heatmap); Comparative Toxicogenomics Database analysis indicated that it was associated with clinical features such as aggressive tumors. Immune infiltration analysis revealed significant heterogeneity in the composition of immune cells in esophageal cancer samples. AURKB is a key driver gene in esophageal cancer, promoting tumor progression through dual mechanisms of cell cycle regulation and ferroptosis resistance. This study not only provides a novel theoretical basis and potential molecular targets for targeted therapy, but also offers valuable insights for precision nursing interventions, particularly in perioperative care, clinical risk assessment, and postoperative rehabilitation of patients with esophageal cancer.
Insights
Aurora kinase B (AURKB) is a key driver in esophageal cancer, promoting tumor growth via cell cycle regulation and ferroptosis resistance. This finding offers new targets for precision therapies and nursing interventions.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Esophageal cancer is a heterogeneous malignancy with poor prognosis and unclear molecular drivers.
- The role of Aurora kinase B (AURKB) in esophageal cancer progression, including its expression and functional mechanisms, remains largely unelucidated.
- Understanding these mechanisms is crucial for developing effective targeted therapies and improving patient care.
Purpose of the Study:
- To identify key molecular drivers and pathways involved in esophageal cancer progression using integrated bioinformatics analysis.
- To investigate the expression characteristics and functional role of AURKB in esophageal cancer.
- To explore potential molecular targets for precision medicine and inform nursing interventions.
Main Methods:
- Utilized public datasets (GSE164158, GSE17351) to screen differentially expressed genes (DEGs) between esophageal cancer and normal tissues.
- Performed functional enrichment analysis (GO, KEGG, GSEA, Metascape) and constructed protein-protein interaction (PPI) networks.
- Integrated weighted gene co-expression network analysis (WGCNA) with DEG analysis and identified core genes using multiple algorithms.
- Analyzed immune infiltration using CIBERSORT and validated AURKB expression and associations.
Main Results:
- Identified 1500 DEGs significantly enriched in cell cycle, DNA replication, and mitosis pathways.
- Integrated network analyses pinpointed 4 core genes, including AURKB, which was highly expressed in esophageal cancer.
- AURKB expression correlated with aggressive tumor features, and immune infiltration analysis revealed significant heterogeneity.
- AURKB promotes esophageal cancer progression via cell cycle regulation and ferroptosis resistance.
Conclusions:
- AURKB is identified as a key driver gene in esophageal cancer, influencing tumor progression through cell cycle control and ferroptosis resistance.
- This study provides a theoretical foundation and potential molecular targets for targeted esophageal cancer therapies.
- Findings offer insights for precision nursing interventions, including perioperative care, risk assessment, and rehabilitation.
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