Figure 7.

Involvement of MAPK signalling in bepridil‐induced cell cycle arrest and apoptosis. (a) Top panel, U87 cells were treated with DMSO (0.1/%, vol/vol), CC‐930 (10 μM), and PD169316 (10 μM) for 18 hr. Lower panel, cells were treated with bepridil (25 μM) alone or pretreated with CC‐930 (10 μM) and PD169316 (10 μM) for 2 hr and then incubated with bepridil for 18 hr. (b) Cell fractions in G₀/G₁, S, and G₂/M phases of each group. Bepridil‐induced G₀/G₁ cell cycle arrest was rescued by PD169316 but not CC‐930. *P < .05, cell fraction in G₀/G₁ phase of PD169316 + bepridil‐treated group versus bepridil‐treated group. n = 5 independent experiments; data were analysed by one‐way ANOVA. (c, d) CC‐930 (10 μM) or PD169316 (10 μM) alone did not increase apoptosis in U87 cells. Cells were pretreated with CC‐930 or PD169316 for 2 hr and then incubated with bepridil (25 μM) for 24 hr; only CC‐930 significantly suppressed bepridil‐induced apoptosis. *P < .05, apoptotic cell fraction in CC‐930 + bepridil group versus bepridil group. n = 5 independent experiments; data were analysed by one‐way ANOVA