Identification and functional exploration of hub genes related to energy metabolism in acute myeloid leukemia.

[OBJECTIVES] Acute myeloid leukemia (AML) is an aggressive hematological malignancy with poor prognosis. Abnormal energy metabolism is a well-recognized cancer hallmark, yet the role of energy metabolism-related genes (EMRGs) in AML remains unclear. Thus, this study aims to identify such hub genes in AML and explore their prognostic significance, related pathways, and therapeutic targeting potential.

[METHODS] AML-related datasets and EMRGs were obtained from public databases. The hub gene was identified through differential expression analysis, correlation analysis and PPI analysis, etc. Then, a set enrichment analysis was conducted. A drug-gene network was constructed, and immune microenvironment analysis was performed.

[RESULTS] In this study, six hub genes (CDH1, AGRN, NDST3, GPC3, CD44, and COL4A1) were identified, and their expression levels were significantly associated with the overall survival of AML patients. These hub genes also exhibited significant expression differences among clusters; for instance, CD44 was upregulated in cluster 2, while COL4A1 and GPC3 were downregulated. Functional enrichment analysis showed that they were associated with 'ribosome', ECM-receptor interaction', and other functional pathways. Consequently, lapatinib, gentamicin, etc., were predicted based on the hub genes, and we found that CDH1 was positively correlated with multiple cells, such as NK cells and T cells, and there was the highest positive correlation between CDH1 and NK cells.

[DISCUSSION] AML shows a poor response to chemotherapy. Six hub genes linked to metabolism, pathways (ribosome, immune, NOD), and drug targets (e.g. Lapatinib/CDH1) were identified. Correlation of CDH1 with NK cells is discussed.

[CONCLUSION] These hub genes offer promising targets for future individualized AML therapy.