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. 2020 Jun 5;21(11):4050. doi: 10.3390/ijms21114050

Figure 4.

Figure 4

Compound L3 suppressed DENV and ZIKV replication through the HER2 signaling pathway. (A–C) MCF-7 cells were infected with DENV-1 for 36 h (A), DENV-2 for 30 h (B), or ZIKV for 36 h (C) (MOI = 1) and treated with 10, 20, or 40 μM of compound L3 to monitor the phosphorylation of HER2, Src, and ERK1/2 signaling molecules by Western blotting. Relative ratios of p-HER2, p-Src, and p-ERK1/2 levels to HER2, Src, and ERK1/2 levels were adjusted to those of the mock control. Viral protein levels were also determined by Western blot analysis. The relative ratios of viral NS3 or E protein levels to actin or GAPDH levels were adjusted to those of the solvent control. Actin or GAPDH was used as the loading control. (D–F) Viral titers in culture supernatants were measured by a focus-forming assay. Data are the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01 by a two-tailed Student’s t-test. (G,H) MCF-7 cells were transiently transfected with an siRNA-HER2 (siHER2) or an siRNA negative control (siNC). At 24 h after transfection, the cells were infected with DENV-2 (G) or ZIKV (H) (MOI = 1) for 24 h and lysed for Western blot analysis. GAPDH was used as a loading control. The relative ratios of viral NS3 or E protein levels to GAPDH levels were adjusted to those of the solvent control.