ArticleFrontiers in genetics2024
Bioinformatics insights into the role of GFPT1 in breast invasive carcinoma: implications for tumor prognosis, immune modulation, and therapeutic applications.
Article in Frontiers in genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Targeted Delivery of GLUT1 Inhibitor via Macrophage Nanovesicles for Pulmonary Arterial Hypertension Therapy.Journal of extracellular vesicles · 2026Article
- Editorial: Screening and discovering novel biological biomarkers by omic-data to revolutionize tumor management.Frontiers in genetics · 2025Article
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Authors and funding
9 authors.
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Abstract
Background: Metabolic reprogramming is a hallmark of cancer, including alterations in the hexosamine biosynthesis pathway (HBP). Glutamine-fructose-6-phosphate transaminase 1 (GFPT1) is the key regulatory enzyme in the HBP; however, its role in invasive breast carcinoma remains underexplored. Methods: This study utilized integrated data from The Cancer Genome Atlas (TCGA) to assess GFPT1 expression in breast cancer (BRCA) patients. Functional enrichment and mutational landscape analyses were performed, along with chemosensitivity predictions. Results: Elevated GFPT1 expression was linked to advanced-stage breast cancer and identified as an independent prognostic marker for overall survival (OS). High GFPT1 levels were associated with increased cytoplasmic translation, activation of oncogenic pathways, and infiltration of M2 macrophages. The GFPT1-High group also showed a higher mutational burden, with frequent TP53 mutations. Chemosensitivity analysis revealed increased IC50 values for chemotherapy drugs in this group. GFPT1 silencing led to reduced cell proliferation and migration, along with enhanced apoptosis. Conclusion: These findings indicate that GFPT1 is a novel prognostic biomarker and a predictive indicator of chemotherapy response in invasive breast carcinoma. GFPT1 influences mRNA translation, cell cycle regulation, and M2 macrophage infiltration, thereby promoting cancer cell proliferation and metastasis.
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