The Role of Interleukin-6 (IL-6) in Lung Cancer Progression and Its Modulation by Anesthetic Agents: A Literature Review

Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with inflammation playing a critical role in its pathogenesis and progression. Interleukin-6 (IL-6) is a multifunctional cytokine that serves as a key molecular bridge between chronic inflammation, angiogenesis, and tumor proliferation. Elevated IL-6 levels are closely associated with advanced tumor stage, metastasis, and poor prognosis in non-small cell lung cancer (NSCLC). During surgery, anesthetic agents and surgical stress can significantly influence IL-6 expression, thereby modulating the tumor microenvironment. Volatile inhalational anesthetics, particularly sevoflurane and isoflurane, have been shown to enhance IL-6 production via activation of nuclear factor-kappa B (NF-κB) and hypoxia-inducible factor-1α (HIF-1α) pathways, promoting angiogenesis, epithelial–mesenchymal transition, and tumor invasiveness. Conversely, propofol-based total intravenous anesthesia (TIVA) exerts anti-inflammatory and antitumor effects by suppressing NF-κB and JAK/STAT3 signaling and reducing IL-6 synthesis, while preserving immune function and natural killer cell activity. These findings highlight IL-6 as a pivotal biomarker and mechanistic link between anesthesia and cancer biology. Understanding how anesthetic techniques modulate IL-6 may lead to more targeted perioperative strategies, potentially improving oncologic outcomes in lung cancer patients. The emerging field of onco-anesthesiology underscores the importance of integrating molecular and immunologic considerations into anesthetic planning for thoracic malignancies.