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. 2020 Jul 7;20:629. doi: 10.1186/s12885-020-07119-2

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© The Author(s) 2020

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Suggested mechanism of action of JB in AML cells. JB in AML exerts its effect through increasing ROS level that cause c-Jun/JNK activation as well as DNA damage. JB also targets PLK1 that contributes to G2/M arrest. Activated c-Jun/JNK may contribute to microtubule disruption and ultimately G2/M arrest. JB was reported to bind directly to the colchicine site on microtubule and inhibits microtubule polymerisation but this was not tested in this study