Fig. 3: YLT-11 induced aberrant centriole duplication in breast cancer cells. | Cell Death & Disease

Fig. 3: YLT-11 induced aberrant centriole duplication in breast cancer cells.

From: YLT-11, a novel PLK4 inhibitor, inhibits human breast cancer growth via inducing maladjusted centriole duplication and mitotic defect

Fig. 3

a MDA-MB-468 and MDA-MB-231 were treated with YLT-11 with an increasing concentration for 24 h, and the centrioles and centrosomes were determined by immunostaining for centrin 2 (green fluorescent staining) and γ-tublin (red fluorescent staining), respectively. DNA was marked by DAPI. Insets show higher magnification views of the centrioles at the spindle pole (boxed regions). Scale bars, 5 μm; 1 μm for insets. b The relative number of cancer cells with abnormal centrioles after treatement with YLT-11 for 24 h, compared with the vehicle group, were counted. Columns, means (n = 3); bars, standard deviation (*p < 0.05, **p < 0.01). c Expression of p-PLK4 was determined by Western blotting. MDA-MB-468 and MDA-MB-231 were treated with DMSO or the indicated concentrations of YLT-11 (0.25, 0.5, and 1 μM) for 48 h, and the expressions of p-PLK4 and PLK4 were detected with a specific antibody. Each has the expression of β-actin as the internal control. Protein expression was quantified by densitometry analysis using ImageJ and normalized against β-actin expression. Columns, mean; bars, SD, *p < 0.05. d Electron micrographs showed the number of centrioles in cells treated with 1 μM YLT-11 for 48 h (right panels), whereas the DMSO group showed only two centrioles (right panel). Scale bar, 500 nm

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