Propofol disrupts cell carcinogenesis and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer
Huaping Zhao, Wei Hua, Juan He, Dongmei Wang, Weihao Li, Yanping Wang, Yanqiu Ai, Jianjun Yang
Abstract
. Propofol decreased the level of circTADA2A and exerted anti-tumor effects by regulating circTADA2A. MiR-455-3p directly interacted with circTADA2A and FOXM1 in lung cancer cells, and circTADA2A could regulate FOXM1 expression by binding to miR-455-3p. Subsequently, rescue assay showed that propofol inhibited cell proliferation, migration, invasion and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer. Collectively, propofol suppressed cell carcinogenesis and aerobic glycolysis by regulating circTADA2A/miR-455-3p/FOXM1 axis in lung cancer, providing an effective clinical implication for propofol to prevent the development of lung cancer.