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. 2016 Dec 8;16:91. doi: 10.1186/s12935-016-0367-5

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© The Author(s) 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 7 — Cell cycle analysis of MCF-7 and MDA-MB231 cells exposed to ESE-15-ol with- and without 3MA. Cells were exposed to DMSO as a negative vehicle control (ai, aii) which showed a prominent G₁ phase. Actinomycin D (bi, bii) was used as a positive control for apoptosis which resulted in an increase in the sub-G₁ phase. An increase in the G₂/M phase was seen in ESE-15-ol-treated cells (ci, cii) with a concurrent decrease in the G₁ phase. ESE-15-ol treated cells together with 3MA (di, dii) showed a decrease in the G₂/M phase with an increase in the G₁ phase. Graphical representation of ei MCF-7 and eii MDA-MB-231 cell cycle analysis. ESE-15-ol-treated cells together with 3MA demonstrated an increase in the G₁ phase when compared to ESE-15-ol-treated cells (P value <0.05; standard deviation represented by T-bars; *indicates statistical difference between compounds and DMSO vehicle control; ^#indicates statistical difference between ESE-15-ol and ESE-15-ol with 3MA)