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eISSN: 1643-3750

Isoflurane Promotes Non-Small Cell Lung Cancer Malignancy by Activating the Akt-Mammalian Target of Rapamycin (mTOR) Signaling Pathway

Wenhua Zhang, Xueqian Shao

Department of Anesthesiology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China (mainland)

Med Sci Monit 2016; 22:4644-4650

DOI: 10.12659/MSM.898434

Available online:

Published: 2016-11-29

BACKGROUND: Lung cancer is one of the leading causes of cancer mortalities worldwide, and non-small cell lung cancer (NSCLC) accounts for the majority of all lung cancer cases. Surgery remains one of the front-line treatment options for NSCLC, but events within the perioperative period were found to affect cancer prognosis, such as anesthesia procedures. Isoflurane, a commonly used volatile anesthetic, enhances the malignant potential of renal, prostate, and ovarian cancer cells, but its effects on NSCLC development have not been previously reported.
MATERIAL AND METHODS: CCK-8 and MTT cell proliferation assays were used to analyze NSCLC cell proliferation. Metastatic ability was examined by wound healing and transwell assays. We used Western blot analysis to study the mechanism of effect of Isoflurane in NSCLC development.
RESULTS: We demonstrated that isoflurane promotes proliferation, migration and invasiveness of NSCLC cells, as well as upregulation of the Akt-mTOR signaling pathway in NSCLC cells. Pharmacological inhibition of Akt-mTOR signaling abolished the ability of isoflurane to promote proliferation, migration, and invasion of NSCLC cells, indicating that isoflurane promotes NSCLC cell malignancy by activating the Akt-mTOR signaling pathway.
CONCLUSIONS: Isoflurane promotes NSCLC proliferation, migration and invasion by activating the Akt-mTOR signaling pathway.

Keywords: Cell Line, Tumor, Carcinoma, Non-Small-Cell Lung - pathology, A549 cells, Cell Movement - drug effects, Cell Proliferation - drug effects, Isoflurane - toxicity, Lung Neoplasms - pathology, Proto-Oncogene Proteins c-akt - metabolism, Signal Transduction - drug effects, TOR Serine-Threonine Kinases - metabolism