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Figure 1. Artemisinin derivatives inhibited EOC growth and arrested the cell cycle at the G2/M phase (A) SKOV3 and primary epithelial ovarian cancer (EOC)

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Presentation on theme: "Figure 1. Artemisinin derivatives inhibited EOC growth and arrested the cell cycle at the G2/M phase (A) SKOV3 and primary epithelial ovarian cancer (EOC)"— Presentation transcript:

1 Figure 1. Artemisinin derivatives inhibited EOC growth and arrested the cell cycle at the G2/M phase (A) SKOV3 and primary epithelial ovarian cancer (EOC) cells were treated with different concentrations of the artemisinin derivatives artesunate (ART) and dihydroartemisinin (DHA) for 24 h. CCK-8 assay showed that ART (a, c) and DHA (b, d) caused dose-dependent cell viability inhibition in both cell lines (n = 6). (B) The proportions of cells in various cell cycle phases were analyzed by flow cytometry for the SKOV3 cell line (a, b) and primary EOC cells (c, d) (n = 3, performed in triplicate). Cells were treated with 0, 30, and 50 μM ART (a, c) or DHA (b, d) for 24 h. Both ART and DHA increased the cell population percentage in the G2/M phase in SKOV3 cells (a, b) and primary EOC cells (c, d). The flow cytometry analysis diagrams are shown in Supplementary Fig. S1C. (C) Apoptotic cells (annexin-V-positive and propidium iodide (PI)-negative for early apoptosis and annexin-V-positive and PI-positive for late apoptosis) were analyzed by flow cytometry. SKOV3 cells (a–f) and primary EOC cells (g–l) were treated with 30 μM or 50 μM ART or DHA, which caused cell cycle arrest. The x-axis represents annexin-V-FITC fluorescence, and the y-axis represents PI fluorescence. The apoptosis rates were evaluated (f, l). No significant apoptosis was observed. Data are shown as the mean ± SD. *P < 0.05, **P < 0.01, ***P < NS, not significant. From: Artemisinin derivatives inhibit epithelial ovarian cancer cells via autophagy-mediated cell cycle arrest Acta Biochim Biophys Sin (Shanghai). Published online November 03, doi: /abbs/gmy125 Acta Biochim Biophys Sin (Shanghai) | © The Author(s) Published by Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. All rights reserved. For permissions, please article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model ( 1


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