Local anesthetics have played a transformative role in modern medicine, enabling safe and efficient surgical procedures. Lidocaine, a local agent which was first introduced in 1943 by two Swedish chemists, remains one of the most widely used anesthetics due to its rapid onset, intermediate duration of action, and favorable safety profile.
Lidocaine functions as an amide-type anesthetic affecting multiple ion channels - potassium, calcium, TRP, and HCN channels - as well as various receptors including glutamate, acetylcholine, and G-protein coupled receptors. Research suggests associations between perioperative lidocaine administration and reduced cancer recurrence and enhanced survival in certain malignancies.
Cancer cells aberrantly express NaV1.5 sodium channel variants that promote persistent sodium influx, driving tumor invasion and metastasis. By blocking this variant, lidocaine may slow cancer progression.
Studies show lidocaine suppresses growth and migration in glioma and breast cancer cells through TRPM7 channel blockade. Additionally, lidocaine activates TRPV1 genes, elevating intracellular calcium concentrations and triggering apoptosis in glioma cells and pyroptosis in glioblastoma cells.
While these findings highlight lidocaine's potential as an oncologic adjuvant, further mechanistic studies and large-scale clinical trials are needed to clarify its role and optimize its application in perioperative oncology care.