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. 2020 Apr 28;21(9):3126. doi: 10.3390/ijms21093126

Figure 3.

Figure 3

Drug-specific enhancing effect of cytotoxicity by GANT61 and involvement of the Ras–Raf–MEK–ERK pathway in the regulation of GLI expression in undifferentiated HCC cells. Cell viability assays of HLE (a) and HLF (b) cells treated with 10 μM of GANT61 in combination with various concentrations of anticancer drugs. After 48 h, cell viability was measured by WST assay and is expressed as the percentage of drug-free control. (c) Western blot analysis of phospho-MEK (Ser2017/221), total MEK, and phospho-ERK (Thr202/Tyr204) in the lysate extracted from the cells treated with U1026 (1 μM) and sorafenib (Sora) (10 μM) for 24 h. β-Actin served as a control of protein loading. (d) Relative protein expression levels were calculated from the band intensity with ImageJ software (NIH). (e) Relative gene expression levels of GLI1, GLI2, and GLI3 in U1026- and sorafenib-treated cells compared to the control (DMSO). * p < 0.05, ** p < 0.01 vs. the vehicle control (DMSO).