Research Paper Volume 12, Issue 14 pp 14341—14354

LKB1 inactivation leads to centromere defects and genome instability via p53-dependent upregulation of survivin

Figure 8. LKB1 deficiency sensitizes cells to the survivin inhibitor YM155. (A) Determination of cell viability (MTT assay) in U2OS/sh-Ctrl and U2OS/sh-LKB1 cells treated for 24 h with 10 μM YM155. (B) Western blotting detection of caspase-3 expression in U2OS/sh-Ctrl and U2OS/sh-LKB1 cells treated with YM155 (24 h, 10 μM). (C) Assessment of colony-forming efficiency in U2OS/sh-Ctrl and U2OS/sh-LKB1 cells. Cells were treated with 10 μM YM155 keeping or vehicle and allowed to grow for 10-14 days. Colonies containing at least 50 cells were counted. Data are mean ± SD (n=3).