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. 2012 May;32(10):1879–1892. doi: 10.1128/MCB.06214-11

Fig 4.

Fig 4

Mcl-1 is unique among Bcl-2 family members in its ability to induce senescence in p53− cells. (A) Percentages of SA-β-gal+ HCT116 p53− cells expressing a shRNA specific for Bcl-2 or an irrelevant control after 6 days culture with or without doxorubicin. Western blot verification of the knockdown of Bcl-2 expression. (B) Percentages of SA-β-gal+ HCT116 p53− shControl cell line or HCT116 p53− shMcl-1 cell line plus vector control, overexpressing exogenous Bcl-2, Bcl-xL, Mcl-1, Mcl-1 with a deleted C-terminal/transmembrane mitochondrial targeting domain (Mcl-1ΔC), and Mcl-1 with a mutated BH3 binding groove (BH3) grown for 6 days with or without doxorubicin. Values represent the mean ± SD of at least three independent experiments. Western blot verification of exogenous gene expression in each cell line. (C) Percentages of SA-β-gal+ HCT116 p53+ cells with control vector or overexpressing exogenous Bcl-2, Bcl-xL, Mcl-1, Mcl-1ΔC, or BH3 mutant Mcl-1 grown in media for 6 days with or without doxorubicin. No significant differences were observed between normal Mcl-1 overexpression and the two mutant versions of the Mcl-1 molecule. Values represent the mean ± SD of at least three independent experiments. Western blot verification of protein overexpression in each cell line. (D) Percentages of SA-β-gal+ HCT116 cells after 6 days of growth in media alone or with ABT-737 or AT-101 and with or without doxorubicin. Values represent the mean ± SD of at least three independent experiments. (E) Western blot analysis of Mcl-1 expression after treatment with ABT-737 for the indicated time points.