@Article{or.2026.082954,
AUTHOR = {Xiangui Liu, Jianhua Liu, Qingbin Meng, Yongsheng Shao},
TITLE = {Sevoflurane Inhibits Colon Cancer Progression by Inducing Cell Autophagy and Apoptosis through the ROS/Nrf2/P62 Pathway},
JOURNAL = {Oncology Research},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/or/online/detail/27880},
ISSN = {1555-3906},
ABSTRACT = {<b>Objectives:</b> There is debate over the effect of sevoflurane (SEV) on different cancers. This study aims to explore SEV’s role in colon cancer (CC) progression. <b>Methods:</b> The CC cell lines were treated with SEV at concentrations of 1.7%, 3.4%, and 5.1%. Cell proliferation, apoptosis, migration, and invasion were assessed using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU) incorporation, colony formation assay, flow cytometry, Western blot, scratch assay, and Transwell assay. A xenograft tumor model was established to evaluate the effect of SEV <i>in vivo</i>. Expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2), p62 (sequestosome-1), microtubule-associated protein 1 light chain 3 isoform II to I ratio (LC3-II/I), Beclin-1, Bcl-2-associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2) were measured. N-acetyl-L-cysteine (NAC), a ROS scavenger, was applied to determine whether ROS-dependent Nrf2/p62 signaling participated in this process. <b>Results:</b> SEV inhibited CC cell proliferation, colony formation, migration, and invasion. At 5.1% SEV, cell proliferation was reduced by 54.0% (<i>p</i> < 0.001); colony formation decreased by 55.0% (<i>p</i> < 0.001); and wound closure rates dropped from 78.3% to 24.6% (<i>p</i> < 0.001) in HCT116 cells. Similar trends were observed in SW480 cells. Invaded cells were also significantly reduced in both cell lines (<i>p</i> < 0.001). SEV also induced CC apoptosis. In the xenograft model, treatment with SEV significantly suppressed tumor progression, as evidenced by reductions in both tumor volume and weight (<i>p</i> < 0.001). Mechanistically, SEV increased the LC3-II/I ratio and Beclin-1 expression, while decreasing Nrf2 and p62 expression both <i>in vitro</i> and <i>in vivo</i>. Moreover, NAC reversed the SEV-induced effects <i>in vitro</i>. <b>Conclusion:</b> SEV inhibits CC progression by inducing autophagy and apoptosis via the ROS/Nrf2/p62 pathway.},
DOI = {10.32604/or.2026.082954}
}