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Fig. 2 | Genome Medicine

Fig. 2

From: Targeting CDC7 potentiates ATR-CHK1 signaling inhibition through induction of DNA replication stress in liver cancer

Fig. 2

Effects of ATR and CHK1 inhibitors on HCC cells. a Long-term colony formation assays of a panel of liver cancer cell lines treated with increasing concentrations of AZD6738 (ATR inhibitor, left panel) or MK-8776 (CHK1 inhibitor, right panel) for 10–14 days. Cell lines indicated in red are sensitive to ATR or CHK1 inhibitors, in purple are intermediate sensitive and blue cell lines are resistant to ATR or CHK1 inhibitors. b, c IncuCyte cell proliferation assays of ATR or CHK1 inhibitors sensitive cells (Huh7 and MHCC97H) and resistant cells (SNU449 and PLC/PRF/5) in the presence or absence of 1.25 μM AZD6738 (ATR inhibitor) or 0.625 μM MK-8776 (CHK1 inhibitor) for 6–8 days. d Representative images of AZD6738 (upper panel) or MK-8776 (lower panel) treated HCC cells in the presence of a green fluorescent caspase-3/7 activatable dye. e Western blot analysis of γH2AX as a DNA damage marker in sensitive cells (Huh7 and MHCC97H) and resistant cells (SNU449 and PLC/PRF/5) in the presence or absence of 1.25 μM AZD6738 or 0.625 μM MK-8776 for 72 h. β-actin protein level served as a loading control. f Representative neutral-comet assay images from ATR or CHK1 inhibitors sensitive cells (Huh7 and MHCC97H) and resistant cells (SNU449 and PLC/PRF/5) treated with 1.25 μM AZD6738 or 0.625 μM MK-8776 for 72 h. Tail moment of each treatment group were normalized to the mean tail moment of the control cells. n = 50 cells per cell line and condition. ***P < 0.001

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