Interplay Between GLUT1 Expression and the Long Non-Coding RNA NEAT1 in Breast Cancer

Background: Breast cancer progression is closely linked to metabolic reprogramming and regulatory networks involving non-coding RNAs. A hallmark of this process is increased reliance on aerobic glycolysis, supported by enhanced glucose uptake through the SLC2A1-encoded transporter GLUT1. The long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) regulates transcriptional control, cellular stress responses, and tumor adaptation. This narrative review summarizes the experimental and clinical evidence on GLUT1 and NEAT1 in breast cancer, with a focus on hypoxia-related signaling, metabolic remodeling, and inflammatory pathways.Conclusion: Available data indicate that GLUT1-mediated glucose uptake and NEAT1-driven stress-adaptive mechanisms independently support glycolytic metabolism, tumor survival, and therapy resistance. Emerging evidence suggests functional convergence via shared regulators, including hypoxia-inducible factors, PI3K/Akt–mTOR signaling, and inflammatory cytokines; however, direct molecular regulation between NEAT1 and GLUT1 remains unresolved. Clarifying this relationship may enable the development of combined metabolic, RNA-based biomarkers and therapeutic strategies for aggressive breast cancer subtypes