Abstract

Propofol, an anesthetic agent with known anticancer properties in various tumor types, holds promise as a potential therapeutic option for glioma. However, the specific functions and underlying mechanisms of propofol in glioma tumorigenesis remain poorly understood. We collected twenty-one glioma tissue samples for analysis. In vitro experiments, including 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide, flow cytometry, Western blot, transwell and wound healing assays, were performed to assess the effects of propofol on glioma cells. We also examined the expression levels of long noncoding ribonucleic acid SET binding factor 2-antisense strand 1, microRNA-373-3p, and pyruvate dehydrogenase kinase 3 through quantitative reverse transcription-polymerase chain reaction and Western blotting. Propofol demonstrated inhibitory effects on glioma cell viability by promoting cell apoptosis and inducing cell cycle arrest. Additionally, propofol suppressed the migratory and invasive capacities of glioma cells. We observed an increased expression of SET binding factor 2-antisense strand 1 in glioma, which was attenuated upon propofol treatment. Furthermore, overexpression of SET binding factor 2-antisense strand 1 weakened the inhibitory effects of propofol on glioma progression. MicroRNA-373-3p was identified as a target of SET binding factor 2-antisense strand 1, and its up-regulation counteracted the functional impact of SET binding factor 2-antisense strand 1 in glioma cells treated with propofol. Additionally, we found that microRNA-373-3p targeted pyruvate dehydrogenase kinase 3 and knockdown of microRNA-373-3p reversed propofol-mediated suppression of glioma progression by increasing pyruvate dehydrogenase kinase 3 expression. Our findings suggest that propofol exerts inhibitory effects on glioma cell oncogenic phenotypes through the SET binding factor 2-antisense strand 1/microRNA- 373-3p/pyruvate dehydrogenase kinase 3 axis. This study sheds light on the potential application of propofol in glioma prevention and provides valuable insights into the molecular mechanisms underlying its antitumor properties in this challenging malignancy.