Abstract
Volatile anesthetics are widely used inhalation anesthetics in clinical anesthesia. In recent years, the regulation of anti-cancer relevant signaling of volatile anesthetics has drawn the attention of investigators. However, their underlying mechanism remains unclear. This review summarizes the research progress on the regulation of anti-cancer relevant signaling of volatile anesthetics, including sevoflurane, desflurane, xenon, isoflurane, and halothane in vitro, in vivo, and clinical studies. The present review article aims to provide a general overview of regulation of anti-cancer relevant signaling and explore potential underlying molecular mechanisms of volatile anesthetics. It may promote promising insights of guiding clinical anesthesia procedure and instructing enhance recovery after surgery (ERAS) with latent benefits.
Highlights
Cancer describes diseases characterized by uncontrolled cell division and tissue invasion
This review summarized the regulation of anti-cancer relevant signaling, including anti-proliferation, anti-migration and invasion, anti-metastasis, apoptosis-inducing effects, and the underlying mechanisms of volatile anesthetics
Sevoflurane preconditioning (1.5%, 2.5%, or 3.5% sevoflurane incubation of A549 cells for 4 h) can inhibit the proliferation and invasion of lung cancer A549 cells induced by hypoxia, which may be related to the down-regulation of HIF-1a and its downstream genes X-linked inhibitor of apoptosis (XIAP), survivin, fascin, and HPA [55]
Summary
Cancer describes diseases characterized by uncontrolled cell division and tissue invasion. This review summarized the regulation of anti-cancer relevant signaling, including anti-proliferation, anti-migration and invasion, anti-metastasis, apoptosis-inducing effects, and the underlying mechanisms of volatile anesthetics. It may be instructive for future clinical inhalation anesthesia and beneficial for ERAS. Yi and colleagues reported that sevoflurane inhibited glioma migration and invasion by up-regulating miRNA-637 and suppression of downstream Akt expression and activity [37]. Sevoflurane preconditioning (1.5%, 2.5%, or 3.5% sevoflurane incubation of A549 cells for 4 h) can inhibit the proliferation and invasion of lung cancer A549 cells induced by hypoxia, which may be related to the down-regulation of HIF-1a and its downstream genes XIAP, survivin, fascin, and HPA [55].
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