ArticleFrontiers in genetics2025
Prognostic and tumor microenvironmental features of gastric cancer revealed by macrophage polarization and protein lactylation-related genes.
Article in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Lactylation in gastric cancer: From mechanisms to clinical applications (Review).Molecular medicine reports · 2026Review
- Metabolic Signaling Meets Epigenetic Regulation: How Protein Lactylation Remodels the Tumor Immune Microenvironment in Gastric Cancer.Current issues in molecular biology · 2026Review
- ERCC6L in human cancers: oncogenic functions, molecular mechanisms, and clinical implications as a prognostic biomarker and therapeutic target.Frontiers in oncology · 2026Review
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Authors and funding
9 authors.
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Abstract
Background: The progression of gastric cancer (GC) is closely linked to macrophage polarization and protein lactylation; however, its underlying mechanisms remain poorly understood. This study aimed to elucidate the molecular mechanisms of GC using transcriptomic analysis. Methods: Candidate genes were identified by intersecting differentially expressed genes with key module genes associated with protein lactylation and macrophage polarization. Protein-protein interaction analysis was performed to uncover interacting genes. Prognostic genes were determined using univariate Cox regression and machine learning techniques, with model accuracy assessed via training and validation datasets. Further, enrichment analysis, immune infiltration profiling, gene mutation analysis, and drug sensitivity assessments were conducted for high- and low-risk groups. Chromosomal localization, gene-gene interaction network analysis, and expression validation of prognostic genes were also performed. Results: Two prognostic genes, ERCC6L and MYB, were identified as significant markers of prognosis through comprehensive analyses. A risk model based on these genes accurately predicted survival in patients with GC. Enrichment analysis revealed pathways such as the muscle myosin complex and adipogenesis as significantly involved in GC. Immune infiltration analysis identified 13 immune cell types, including monocytes, with strong associations to the prognostic genes. TTN, TP53, and MUC16 exhibited the highest mutation rates in both risk groups. Drug sensitivity analysis highlighted AZD.0530, CCT007093, DMOG, JNJ.26854165, and LFM.A13 as promising therapeutic candidates. ERCC6L is located on chromosome X, while MYB is located on chromosome 6. Gene-gene interaction network analysis revealed interactions between prognostic genes and other key genes. In both datasets, expression of prognostic genes was significantly higher in the GC cohort. Conclusion: This study identified ERCC6L and MYB as key prognostic genes, facilitating the development of a risk model that offers novel insights into potential therapeutic strategies for GC.
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