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. 2022 Jan 1;14(1):210. doi: 10.3390/cancers14010210

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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(A) Schematic figure demonstrating the escaping palbociclib-resistant cells, MCF7-PR and T47D-PR, via various bypass mechanisms. Mitosis of the aforementioned cells could be blocked by eribulin at the G2/M phase. (B) MCF7-PR cells were treated with IC25 concentration of eribulin, palbociclib, or abemaciclib and their combinations for 24 h. Eribulin and palbociclib or eribulin and abemaciclib combinations treatment was sequentially performed without a time gap between the drugs. Cell cycle distribution comparing the efficacy of palbociclib to abemaciclib after combination with eribulin was analyzed by flow cytometry. HR hormone receptor.

(A) Schematic figure demonstrating the escaping palbociclib-resistant cells, MCF7-PR and T47D-PR, via various bypass mechanisms. Mitosis of the aforementioned cells could be blocked by eribulin at the G2/M phase. (B) MCF7-PR cells were treated with IC25 concentration of eribulin, palbociclib, or abemaciclib and their combinations for 24 h. Eribulin and palbociclib or eribulin and abemaciclib combinations treatment was sequentially performed without a time gap between the drugs. Cell cycle distribution comparing the efficacy of palbociclib to abemaciclib after combination with eribulin was analyzed by flow cytometry. HR hormone receptor.