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. 2018 Apr 13;3:9. doi: 10.1038/s41392-018-0010-0

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© The Author(s) 2018

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. 2 — a Time course and dose-dependent inhibition of direct protein substrates of CDKs in C666-1 cells. Roniciclib significantly inhibited phosphorylation of RNA-polymerase II, retinoblastoma, and nucleophosmin. Drug treatment also induced PARP activation, accompanied by a moderate decrease in survivin expression. The expression of proapoptotic proteins such as BAK, which is known to activate caspases, was enhanced along with concomitant increases in activated caspase-3 and p53 and a decrease in the anti-apoptotic protein MCL-1. b Changes in the percentage of dead C666-1 cells over the course of drug incubation. c Apoptosis and FCM analysis of C666-1 cells treated at 10 nM. d Apoptosis and FCM analysis of C666-1 cells treated at 50 nM. c and d indicate cell death and cell cycle arrest via G2/M accumulation and subsequent shifts to G0 by days 3, 7, and 10. P7: G1 phase; P8: S phase; P9: G2/M phase; P10: G0 phase. FCM flow cytometry, EBV Epstein–Barr virus