Abstract
An improved understanding of the cellular mechanisms that account for the protective effect of inhalational anesthetics on tissues subjected to ischemia–reperfusion injury has led some to question whether a similar survival advantage may be afforded to cancer cells in patients undergoing surgery. Such an effect would be potentially detrimental to long-term cancer outcomes. Anesthetic-induced activation of hypoxia-inducible factors and upstream cell signaling pathways such as PI3K/Akt/mTOR appear to underpin the adaptive and pro-survival responses of cells to potentially lethal injuries. These same pathways are heavily implicated in malignancy and metastasis and their activity is associated with poor prognosis in most human solid cancers. This review gives an account of the manner in which inhalational anesthetics amplify cell signaling and induce transcriptional modifications to a variety of cell types, with a particular focus on how this relates to cancer cell biology and the various hallmarks of malignancy such as angiogenesis, cell proliferation, metabolic adaptation, invasion, and metastasis.
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