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. 2021 Feb 11;11:3656. doi: 10.1038/s41598-021-83142-y

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© The Author(s) 2021

Open Access This 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/.

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Impact of CHK1 kinase inhibition on replication stress in KRAS mutant (mut) vs wild-type (wt) cancer cells. (a) Representative immunofluorescence images depicting the effects of pharmacological CHK1 inhibition (Chk1i) with LY2603618 (1 µM) during the second label (IdU) in isogenic NCI-H1703 cancer cells. (b) Frequency distributions of DNA fiber length with and without LY2603618 treatment. (c) Percentage of fibers indicating stalled forks. (d) Percentage of the ratio of new origins fired during the second label (ldU) and overall origin firings during both pulses. (e) Left, representative immunofluorescence images showing nuclear γ-H2AX and DAPI staining in Chk1 inhibitor-treated cells. Right, percentage of cells with at least 5 γ-H2AX foci following 16 h of treatment with LY2603618. All bars represent mean + /- SEM based on 3 independent repeats. Statistical comparisons by two-sided T-test indicating *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001.