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. 2022 Oct 18;22:1073. doi: 10.1186/s12885-022-10119-z

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© The Author(s) 2022

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. 8 — A schematic diagram of working mechanism of SMI#9/PTX combination therapy in TNBC chemosensitization. PTX or SMI#9 treatments induce mitotic arrest which can result in cell death or mitotic slippage. Formation of tetraploid G1 cells, a feature of mitotic slippage, is facilitated by premature cyclin B1 destruction and abnormal mitotic exit without chromosome segregation or cytokinesis. SMI#9 treatment enhances PTX cytotoxicity by inducing monopolar mitotic spindles and strengthening arrest and mitotic catastrophe of cells that slipped out of prolonged mitotic arrest