Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC Cells

Figure 5

JC induces apoptosis by inhibiting the transcriptional activity of Foxo3a. (a, c) Effect of JC on Foxo3a levels in the nucleus was determined by Western blot analysis. HepG2 cells were treated with either DMSO or 8 μg/mL of JC for the indicated times (a). BEL-7402 cells were treated with either DMSO or 8.7 μg/mL of JC for the indicated times (c). Histone H1 was used as a loading control. (b, d) Effect of JC on the Akt/Foxo3a signaling pathway was determined by Western blot analysis. HepG2 cells were treated with either DMSO or 8 μg/mL of JC for the indicated times (b). BEL-7402 cells were treated with either DMSO or 8.7 μg/mL of JC for the indicated times (d). GAPDH was used as a loading control. (e, f) Overexpression of Foxo3a inhibits JC-induced apoptosis. HepG2 and BEL-7402 cells were transiently transfected with pcDNA3 vector control or pcDNA3-Foxo3a. Twelve hours after transfection, HepG2 cells were treated with either DMSO or 8 μg/mL of JC for 36 hours (e). BEL-7402 cells were treated with either DMSO or 8.7 μg/mL of JC for 24 hours (f). Then, cell apoptosis was detected by Western blot analysis. GAPDH was used as a loading control.

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