Journal of Cancer Prevention : pISSN 2288-3649 / eISSN 2288-3657

Fig. 1.

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Fig. 1.

Effect of β-carotene on cell viability, phosphorylation of GSK3β, and expression of β-catenin, c-myc, and cyclin E in gastric epithelial cells with Helicobacter pylori infection. Uninfected cells (column “None”), cells with H. pylori infection in the absence of β-carotene (column “Control”) and in the presence of 5 μM or 10 μM β-carotene (columns β-carotene 5 and 10, respectively). (A) The percentage of viable cells. aP < 0.05 vs. “None”; bP < 0.05 vs. “Control”. All values were expressed as mean ± SE of 3 different experiments (n = 4 per group for each experiment). (B) Left panel: Western blot of β-catenin, glycogen synthase kinase 3β (GSK3β) and phosphorylated glycogen synthase kinase 3β (p-GSK3β). Center panel: ratio of p-GSK3β/total GSK3β calculated from the Western blot. Right panel: the amount of β-catenin calculated from the Western blot and reported in ratio to the gel loading control actin. (C) Left panel: Western blot of c-myc and cyclin E. Center panel: the amount of c-myc calculated from the Western blot and reported in ratio to the gel loading control actin. Right panel: the amount of cyclin E calculated from the Western blot and reported in ratio to the gel loading control actin. aP < 0.05 vs. “None”; bP < 0.05 vs. “Control”. Values are expressed as the mean ± SE of 4 per each group. A P-value of 0.05 or less was considered statistically significant.

J Cancer Prev 2019;24:192-6 https://doi.org/10.15430/JCP.2019.24.3.192
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