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. Author manuscript; available in PMC: 2012 Jun 1.
Published in final edited form as: Mol Cancer Ther. 2011 Apr 25;10(6):960–971. doi: 10.1158/1535-7163.MCT-11-0072

Figure 2.

Figure 2

B7-H3 silencing increased the sensitivity to paclitaxel in breast cancer cells. A, Western blot analysis demonstrating the B7-H3 protein level of MDA-MB-231 (left) and MDA-MB-435 cells (right), expressing either non-target vector control TR33 or shB7-H3 and their corresponding parental cells. β-actin levels served as loading control. B, Cell viability of 231, 231-TR33, 231-shB7-H3 (top), 435, 435-TR33, and 435-shB7-H3 cell variants (bottom) following treatment with paclitaxel at various concentrations for 72 h was assessed using MTS assay. Data are presented as the percentage of cell growth inhibition measured in paclitaxel treated cells compared to untreated cells. The p value shows the difference between paclitaxel-treated B7-H3 knockdown cells and parental cells. Columns, mean of three independent experiments performed in triplicates; bars, S.E.; ** p< 0.01; *** p < 0.001.