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. 2015 Nov 2;11(1):182–188. doi: 10.3892/ol.2015.3854

Figure 5.

Figure 5.

Mitogen-activated protein kinase signal pathways may partially be involved in the anti-tumor activity of BCTC towards DU145 cells. (A) DU145 cells were treated with various concentrations of BCTC for 48 h. Western blot analysis was performed to investigate the expression of p-p38, p38, p-ERK1/2, ERK1/2, p-JNK and JNK. (B) Western blot analysis was quantified and a one-way analysis of variance was performed. (C) DU145 cells were pre-treated with a p38 inhibitor (SB203580; 20µM) and a JNK inhibitor (SP600125; 10 µM) for 4 h, and then treated with 100 µM BCTC. After 48 h treatment, cell viability was determined by a MTT assay. Experiments were performed in triplicate. Western blot analysis was quantified and one-way analysis of variance was performed. Error bars indicate the mean ± standard deviation. *P<0.05, **P<0.01 and ***P<0.001 vs. control; #P<0.05 vs. BCTC group. BCTC, N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)piperazine-1-carboxamide; p-ERK, phosphoryalted extracellular signal-regulated kinase; p-JNK, phosphorylated c-Jun N-terminal kinase; p-p38, phosphorylated p38.