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. 2021 Apr 14;12(4):395. doi: 10.1038/s41419-021-03665-0

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© The Author(s) 2021

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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Fig. 7 — A Representative histograms 48 h post treatment; B cell cycle distribution (top) and percentage of sub/G1 apoptotic cells (bottom); C analysis of caspase 3/7 activity vs. cell survival in OVCAR4 (left panel), Ov4Carbo (middle panel) and summary of assay (right panel). Cells were treated with chloroxine (10 μM), carbo II (100 μM) or combi. II (chloroxine 10 μM + carboplatin 100 μM). Untreated cells were used as control. Data show mean ± s.d., and percentage of G1 (2n), S and G2/M (4n) fraction population (FACs: n = 2; caspase 3/7: n = 3 biological repeats). Unpaired t test, ****P < 0.0001, *P < 0.05 (compared to carboplatin treated).