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. 2023 May 22;24(10):9076. doi: 10.3390/ijms24109076

Figure 5.

Figure 5

Targeting ER stress inhibits fisetin-induced apoptotic cell death in liver cancer cells. (A–C) HepG2 and Hep3B cells were transfected with GRP78 siRNA and treated with fisetin (100 μM, 24 h). LDH activity, Cell viability, and ER stress-related protein (CHOP, PERK, p-PERK, GRP78, and cleaved caspase-3) levels were measured. * = p < 0.05, n.s = no significant. Relative mRNA expression levels were normalized to β-actin. β-actin was used as the protein loading control. (D–F) Cell viability, LDH activity, and ER stress-related protein (cleaved caspase-3, CHOP, PERK, and p-PERK) levels in the HepG2 and Hep3B cells treated with fisetin (100 μM, 24 h) were measured in the presence or absence of PERK siRNA (30 nM, 24 h). * = p < 0.05. β-actin was used as the protein loading control. (G,H) LDH activity, Cell viability, and western blot analyses for CHOP and cleaved caspase-3 in HepG2 and Hep3B cells treated with fisetin (100 μM, 24 h) were performed in the presence or absence of CHOP siRNA (30 nM, 24 h). * = p < 0.05. β-actin was used as the protein loading control. Data are representative of three experiments.