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

Li-Yan Jin; Kui Zhao; Long-Jiang Xu; Rui-Xun Zhao; Kaitlin D. Werle; Yong Wang; Xiao-Long Liu; Qiu Chen; Zhuo-Jun Wu; Ke Zhang; Ying Zhao; Guo-Qin Jiang; Feng-Mei Cui; Zhi-Xiang Xu

doi:doi:10.18632/aging.103473

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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 7. LKB1 suppresses survivin expression via p53. (A) Western blotting detection of survivin in p53WT and p53DN H460 cells after overexpression of LKB1. (B) Western blotting detection of survivin in HCT116/sh-Ctrl and HCT116/sh-LKB1 cells after transfection with mutated P53 (#1-#4) or WT P53 vectors. (C) Western blotting detection of survivin in HCT116(p53^-/^-) and HCT116(p53⁺/⁺) cells transfected with siRNA-Ctrl or siRNA-LKB1. Thirty micrograms of protein per lane were loaded. GAPDH served as loading control. (D) Luciferase reporter assay indicating negative regulation of the survivin promoter by p53.