Background: The overall response rate of immunotherapy in triple-negative breast cancer (TNBC) remains unsatisfactory. Accumulating evidence indicated that glucose metabolic reprogramming could modulate immunotherapy efficacy. However, transcriptomic evidence remains insufficient.
Methods: Genes' relationship with glucose metabolism and TNBC-specific immune was demonstrated by weighted gene co-expression network analysis (WGCNA). The glucose metabolic capability was estimated by standardised uptake value (SUV), an indicator of glucose uptake in 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET), and a reflection of cancer metabolic behaviour. PD-(L)1 expression was used to reflect the efficacy of immunotherapy. Additionally, immune infiltration, survival, and gene coexpression profiles were provided.
Results: Comprehensive analysis revealing that IL4I1, ITGB7, and FUT7 hold the potential to reinforce immunotherapy by reshaping glucose metabolism in TNBC. These results were verified by functional enrichment analysis, which demonstrated their relationships with immune-related signalling pathways and extracellular microenvironment reprogramming. Their expressions have potent positive correlations with Treg and Macrophage cell infiltration and exhausted T cell markers. Meanwhile, their overexpression also lead to poor prognosis.
Conclusion: IL4I1, ITGB7, and FUT7 may be the hub genes that link glucose metabolism, and cancer-specific immunity. They may be potential targets for enhancing ICB treatment by reprogramming the tumour microenvironment and remodelling tumour metabolism.
Keywords: FDG-PET; PD-(L)1; Triple-negative breast cancer; glucose metabolism; immunotherapy.