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. 2019 Dec 13;34(5):1315–1328. doi: 10.1038/s41375-019-0677-4

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© The Author(s) 2019

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. 4 — a Expression of proteins involved in G2/M cell cycle arrest (CDK1, p-Thr161-CDK1, p-Tyr15-CDK1, p-Thr14-CDK1) was assessed by western blotting in Ramos, DOHH2 and Rec-1 cells during and after exposure to 0 (NT) and 6 MBq/mL of ¹⁷⁷Lu-lilotomab for 18 h. Cell proliferation (flow cytometry) and CDK1 phosphorylation at Tyr15 and Thr14 (western blotting) were determined in b Ramos and c DOHH2 cells during and after exposure to 0 (NT) and 6 MBq/mL ¹⁷⁷Lu-lilotomab alone, or with 1 µM MK-1775 (WEE-1 inhibitor) or 1 µM PD-166285 (WEE-1 and MYT-1 inhibitor). Proliferation was calculated as the percentage of the value in nontreated cells (left black bar) set to 100%. Data are the mean ± SD of three independent experiments in triplicate (*p < 0.05).