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. 2018 Sep 13;8:13762. doi: 10.1038/s41598-018-32195-7

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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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The mitotic index of HTLA-ER cells and their Bax/Bcl2 ratio were not modified by acute etoposide exposure. (A) Mitotic index of HTLA-230 and HTLA-ER cells untreated or treated for 24 hrs with 1.25 μM etoposide. Histograms summarize quantitative data of means ± S.D. of four independent experiments per experimental condition (at least 4 × 10³ cells per experimental condition were counted) **p < 0.01 vs. untreated HTLA-230 cells. (B) Protein levels of Bax and Bcl2 in HTLA-230 and HTLA-ER cells untreated or treated for 24 hrs with 1.25 μM etoposide. Immunoblots are representative of three independent experiments with essentially similar results. β-Actin is the internal loading control. The histograms on the left summarize quantitative data of protein level means, normalized to β-actin expression ± S.E.M of three independent experiments. The histograms on the right summarize quantitative data of Bax/Bcl2 ratio means ± S.E.M of three independent experiments. *p < 0.05 vs. untreated HTLA-230 cells; **p < 0.01 vs. untreated HTLA-230 cells; ^§§p < 0.01 vs. untreated HTLA-ER cells.