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. 2021 Feb 9;124(8):1411–1420. doi: 10.1038/s41416-021-01272-6

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© The Author(s), under exclusive licence to Cancer Research UK 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — HROC18 (a), HROC131 T0 M3 (b), HROC147Met (c), HROC277Met2 (d), HROC277 T0 M1 (e), HROC278Met T2 M2 (f), HROC285 T0 M2 (g), HROC370 (h), HROC374 (i), HROC46 T0 M1 (j), HROC50 T1 M5 (k) and HROC87 T0 M2 (l) were treated with appropriate vehicle, 1 µM, 2.5 µM, 6.25 µM or 15.6 µM oxaliplatin (OXA) for 5 days. Oxaliplatin significantly inhibited the cell viability. $ indicates P < 0.001, which was determined by one-way analysis of variance with Holm–Sidak’s post hoc test; * indicates P < 0.05, which was determined by Kruskal–Wallis one-way analysis of variance on Ranks with Tukey’s post hoc test. For (e), (g), (h) and (i), N = 6; for the other cell lines, N = 4.