ArticleBMC cancer2025
Identification and validation of glucose metabolism-related gene signature in endometrial cancer.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Recent updates and future perspectives about ALDH1B1 as a potential anticancer target: a review.Journal of cancer research and clinical oncology · 2025Review
- Biomarkers and immunotherapy in endometrial cancer: mechanisms and clinical applications.Frontiers in immunology · 2025Review
- Navigating tumour microenvironment in endometrial carcinoma: a comprehensive review integrating immunohistochemistry, single-cell RNA-sequencing and spatial transcriptomics.Frontiers in oncology · 2025Review
- Remodeling the tumor microenvironment: regulatory effects of β-sitosterol and luteolin on the immunosuppressive milieu in endometrial carcinoma and implications for combinatorial immunotherapy.Frontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetabolic syndrome associated with glucose metabolism plays a pivotal role in tumorigenesis, potentially elevating the risk of endometrial cancer (EC). This study sought to establish a glucose metabolism-related gene (GMRG) signature linked to EC.
methodsDifferential analysis was conducted to identify differentially expressed genes (DEGs) between EC and normal samples from the TCGA-EC dataset. Glucose metabolism-related DEGs (GMR-DEGs) were then derived by intersecting these DEGs with GMRGs. A prognostic signature for EC was developed through the Least Absolute Shrinkage and Selection Operator (LASSO) regression and univariate Cox analysis. Additionally, immune profiling and immunotherapy responsiveness were evaluated across two distinct risk subgroups, accompanied by a single-cell analysis of prognostic genes. The expression levels of these prognostic genes were quantified at both transcriptional and translational stages using reverse transcription quantitative PCR (RT-qPCR) and immunohistochemistry (IHC) in clinical samples. Furthermore, the functional significance of key genes was explored through in vitro assays.
results2,912 DEGs and 202 GMR-DEGs were identified between the EC and normal groups. Subsequently, six prognostic genes were derived, including ASRGL1, SLC38A3, SLC2A1, ALDH1B1, GAD1, and GLYATL1. EC patients were classified into high and low-risk subgroups based on the six genes. Independent prognostic analysis indicated that risk score and disease stage were significant independent prognostic factors. Single-cell analysis revealed that the six prognostic genes were highly expressed in ciliated and epithelial cells. Immune cell infiltration was generally lower in the high-risk group, where tumor purity was elevated. The expression levels of SLC38A3, SLC2A1, and ASRGL1 are higher in tumor samples by RT-qPCR, with IHC confirming increased SLC38A3 expression. Finally, SLC38A3 may function as oncogenes in EC, as revealed by the results of in vitro experiments.
conclusionsIn this study, we developed six novel prognostic genes in EC based on glycolysis, and corresponding prognostic models were developed. Notably, we identified SLC38A3 as the key gene, which offers valuable insights for further research into EC.
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