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. 2018 Jul;366(1):184–193. doi: 10.1124/jpet.118.249151

Fig. 5.

Fig. 5.

Antagonizing survivin by MX106 leads to cell cycle arrest and abnormal cell division. (A) Survivin was depleted by small interfering RNA in HEK293T cells. NF-κB activation upon VP16 treatment (10 µM, 2 hours) was examined by EMSA as indicated. (B) Cell cycle in control or MX106 treated (3 µM, 48 hours) MDA-MB-231 cells was examined by flow cytometry. (C and D) Mitotic cells and cell division were visualized by immunofluorescence staining with anti-α-tubulin and 4′,6-diamidino-2-phenylindole in control or MX106-treated (2 µM, 48 hours) MDA-MB-231 cells. Representative abnormal microtubule spindles and aberrant cell division upon MX106 treatment are shown in (C) and are quantified as abnormal nuclear events in (D). EMSA, Electrophoretic Mobility Shift Assay.