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. 2021 Oct 18;13:166. doi: 10.1186/s13073-021-00981-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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