FIGURE 1.

Lidocaine plays a crucial role in surgical procedures. Beyond its inherent analgesic effects, it also exhibits multiple inhibitory effects on breast cancer. Research has shown that lidocaine can regulate nuclear substances, exerting inhibitory effects (A). By targeting related channels and receptors on the plasma membrane and mitochondrial membrane, lidocaine inhibits the viability and migration of breast cancer cells (B). Lidocaine reduces lung metastasis by inhibiting Src, which in turn downregulates the expression of MMP-2 and MMP-9 (C). Additionally, lidocaine promotes autophagosome-lysosome formation in breast cancer cells and is involved in caspase-dependent apoptosis signaling pathways (D). When used in combination with other anti-breast cancer drugs, lidocaine enhances the therapeutic efficacy of each agent (E). Lidocaine also downregulates the expression of protein gene product 9.5, neurofilaments, nerve growth factor, and neural components, thereby inhibiting the growth of breast cancer cells (F). Co-culture with tumor-associated macrophages (TAMs) and triple-negative breast cancer (TNBC) cells reveals that lidocaine reduces M2-type TAMs, increases M1-type TAMs, and induces the reprogramming of M2 to M1. This process decreases TGF-β/Smads-mediated epithelial-mesenchymal transition (EMT) signaling, thereby inhibiting cancer metastasis and recurrence (G). Lidocaine also reduces the adhesion of circulating breast cancer cells by inhibiting McTNs (H). (Created with BioRender.com).