Figure 3
Figure 3. Effects of pharmacologic inhibition of SIRT1 on CML cell survival. (A) KCL-22 and K562 cells were treated with 1μM imatinib mesylate (IM) with or without 50μM sirtinol. Surviving cells were counted at 2 and 4 days after the treatment. (B) Apoptosis was analyzed 2 days after drug treatment. KCL-22 cells and BCR-ABL–negative KG-1 cells were treated with 2.5μM IM, whereas K562 cells were treated with 0.25μM IM in the presence or absence of 50μM sirtinol. DMSO was used as control (CTL). (C) KCL-22 cells were treated with DMSO (CTL) or 5 or 10μM tenovin-6 in the absence or presence of 2.5μM IM. Apoptosis was analyzed 3 days after drug treatment. (D) Flow cytometry–based analysis of FOXO1 acetylation in KCL-22 cells after mock, 2.5μM tenovin-6, or 50μM sirtinol treatment. Cells were labeled with anti-acetyl FOXO1 Ab or normal IgG as a control.

Effects of pharmacologic inhibition of SIRT1 on CML cell survival. (A) KCL-22 and K562 cells were treated with 1μM imatinib mesylate (IM) with or without 50μM sirtinol. Surviving cells were counted at 2 and 4 days after the treatment. (B) Apoptosis was analyzed 2 days after drug treatment. KCL-22 cells and BCR-ABL–negative KG-1 cells were treated with 2.5μM IM, whereas K562 cells were treated with 0.25μM IM in the presence or absence of 50μM sirtinol. DMSO was used as control (CTL). (C) KCL-22 cells were treated with DMSO (CTL) or 5 or 10μM tenovin-6 in the absence or presence of 2.5μM IM. Apoptosis was analyzed 3 days after drug treatment. (D) Flow cytometry–based analysis of FOXO1 acetylation in KCL-22 cells after mock, 2.5μM tenovin-6, or 50μM sirtinol treatment. Cells were labeled with anti-acetyl FOXO1 Ab or normal IgG as a control.

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