Reveals lidocaine's impact on lipid metabolism and cancer cell behavior, suggesting repurposing potential.
BACKGOUND: Breast cancer exhibits high heterogeneity and drug resistance, presenting severe challenges in clinical treatment. PURPOSE AND METHOD: This study takes cellular lipid metabolism regulation as the core entry point, integrates network pharmacology and computational biology techniques to mine the breast cancer transcriptome data from the GEO database GSE45827, GSE33447, and TCGA-BRCA database. Combined with molecular docking technology, it verifies the binding characteristics and action mode of lidocaine with the core target proteins. RESULT: The study identified 6 core genes regulated by lidocaine in breast cancer, G6PD, ALB, EDN3, FGF2, MAOB, and DMD, all of which are directly or indirectly related to cellular lipid metabolism regulation. CONCLUSION: This study clarified the core mechanism by which lidocaine regulates the lipid metabolism reprogramming of breast cancer cells through multiple targets, revealed that cellular lipid metabolism regulation is the key pathway for its anti-tumour effect, and provided a metabolic-level theoretical basis for repurposing of lidocaine as an old drug.
No takes yet. Share an insight, caveat, or question.
Ye et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: