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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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Resistance of KRAS mutant (mut) but not wild-type (wt) cancer cells to hydroxyurea (HU). (a) Distribution of fiber length in the isogenic NCI-H1703 pair with and without HU treatment (2 mM) administered for 2 h in between pulse labels. (b) Velocity of fork progression with and without HU treatment. (c, d) Percentage of fibers indicating fork stalling with/without 2 h treatment with HU or the topoisomerase I inhibitor camptothecin (CPT). (e, f) Distribution of fiber length and percentage of fork stalling in isogenic DLD1/DWT7 cells, analogous to panels A and B. (g, h) Combined effects of treatment with HU and CHK1 inhibitor (Chk1i) LY2603618 on fork stalling or γ-H2AX foci formation. All bars represent mean + /- SEM based on at least 3 independent repeats. Statistical comparisons by two-sided T-test indicating *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001; ns, not significant.