Fig. 1: BE and EAC cells display specific mitotic defects. | Cell Death & Differentiation

Fig. 1: BE and EAC cells display specific mitotic defects.

From: Evidence that polyploidy in esophageal adenocarcinoma originates from mitotic slippage caused by defective chromosome attachments

Fig. 1

a Cells from representative BE and OAC cell lines were stained to detect the mitotic marker histone H3 pS10, tubulin and DNA (see f and g below). The percentages of cells in mitosis (mitotic indices) were counted (a) and categorized by each mitotic stage (b) through visual analysis of the presence of H3 pS10 and characteristic mitotic figures. In addition, for each cell line the number of abnormal mitoses was also counted (c) and categorized into one of three phenotypes: lagging chromatin, multipolar spindles, or scattered chromosomes (e). d Graph showing the percentages of multinucleate cells from the experiments described in (ag). More than 3000 cells in total and more than 200 mitotic cells per each cell line were counted; n ≥ 6 independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (Mann–Whitney U test). Two-way ANOVA statistical analyses with multiple comparisons of the data in (b) and (e) are shown in Supplementary Table S2 and S3, respectively. To improve visualization, only the summary of the data is shown in (e), but a similar graph including also the individual values is shown in Supplementary Fig. S1. In each graph, bars indicate SEM. f, g Representative images from the indicated BE and OAC cell lines fixed and stained to detect the mitotic marker histone H3 pS10 (red in the merged images), tubulin (green in the merged images), and DNA (blue in the merged images). Bars, 10 μm.

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