Skip to main content
. 2018 May 2;16(1):402–408. doi: 10.3892/ol.2018.8606

Figure 2.

Figure 2.

Propofol suppresses Wnt signaling in glioma cells. (A) Luciferase reporter assays. LN299 cells were transfected with the SuperTopFlash reporter plasmid. After 24, the cells were treated with indicated concentrations of propofol for 48 h and luciferase activities were measured. Results are shown as the mean ± standard deviation of three independent experiments. *P<0.05. (B) Western blot analysis of protein levels of pLRP6, total LRP6 and total β-catenin in LN299 cells treated with indicated concentrations of propofol for 48 h. Tubulin was used as a loading control. (C) Reverse transcription-quantitative polymerase chain reaction analysis of mRNA levels of CCND1 and BLC2 in LN299 cells treated with indicated concentrations of propofol for 48 h. The mRNA expression was normalized to GAPDH. Results are shown as the mean ± standard deviation of three independent experiments. *P<0.05. (D) Western blot analysis of protein levels of CCND1 and BCL2 in LN299 cells treated with indicated concentrations of propofol for 48 h. Tubulin was used as a loading control. LRP6, lipoprotein receptor-related protein 6; pLRP6, phosphorylated LRP6; CCND1, cyclin D1; BCL2, B-cell lymphoma 2.