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. Author manuscript; available in PMC: 2013 Aug 15.
Published in final edited form as: Cancer Res. 2012 Jun 12;72(16):4225–4237. doi: 10.1158/0008-5472.CAN-12-1118

Figure 1. The pan-Cdk inhibitor flavopiridol (FP) interacts synergistically with the pan-Bcl antagonist obatoclax to induce mitochondria-dependent apoptosis in MM cells.

Figure 1

Human MM U266 cells were exposed (24 hr) to (A) 100 nM FP +/− 500 nM obatoclax (Obat); (B, D) 75 – 100 nM FP +/− 500 – 750 nM obatoclax; or (C) 80 – 110 nM FP +/− 400 – 550 nM obatoclax at a fixed ratio (1 : 5). After drug treatment, cell death and related signaling pathways were analyzed by flow cytometry after stained with (A) DiOC6 (Δψm) and 7AAD (cell death), or (B, C) Annexin V-FITC/PI (early and late apoptosis); and (D) immunoblot for cytosolic S-100, mitochondria-enriched fractions, or for whole cell lysates. β-actin = loading controls for S-100 and whole cell lysate; Bak = loading control for mitochondrial fraction; CF = cleaved fragments.