Sevoflurane Represses the Malignancy of Colorectal Cancer by Regulating the p38/MAPK Pathway

Abstract

Objective: Sevoflurane is an inhalation anesthetic that exhibits a crucial role in cell growth, invasion, and apoptosis across various tumor types. Nevertheless, the underlying molecular mechanism remains largely unknown. Therefore, this study aimed to investigate sevofluranes effects on colorectal cancer (CRC) progression and its underlying mechanisms. Materials and Methods: The SW480 and LOVO cells were divided into two groups: a control group (cells without treatment) and a sevoflurane group (cells treated with 4% sevoflurane for 6 hours). Cell viability, proliferation, and clone formation ability were determined through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 5-Ethynyl-2′-deoxyuridine (EdU), and clone formation assays, respectively. Moreover, metastasis in these cells was determined using transwell and wound healing assays. Furthermore, flow cytometry was utilized to assess cell apoptosis rate. Additionally, Western blot assay was employed to determine the p38/mitogen-activated protein kinases (MAPK) pathway. Results: Sevoflurane hindered CRC cell proliferation, clone formation, and metastasis while promoting apoptosis. Mechanically, sevoflurane restrained the p38/MAPK pathway in CRC cells. However, p38/MAPK agonist dehydrocorydaline (DHC) restored the inhibitory effect of sevoflurane on the cell function. Conclusion: These results uncover an antitumor activity of sevoflurane on the invasion and migration of CRC through the p38/MAPK pathway, offering a novel mechanism for studying surgery-mediated CRC treatment.