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. Author manuscript; available in PMC: 2014 Jan 20.
Published in final edited form as: Cancer Res. 2008 Jun 1;68(11):4369–4376. doi: 10.1158/0008-5472.CAN-07-6559

Figure 6.

Figure 6

Mechanism by which 6BT can induce differentiation. A, phosphorylation of 6BT is essential for its activity. HL-60 cells were treated with 6BT alone or in combination with the specific adenosine kinase inhibitor, 5 iodotubericidin for 4 d, and the NBT reduction assay was performed as described in Fig. 2. Results are an average of three independent experiments. B, 6BT potently depletes ATP stores in leukemic cells. HL-60, OCI-AML3, and MV411 cells were treated for the indicated time points with 6BT, ATRA, or vehicle. An equal number of viable (as measured by trypan blue) cells was assessed for ATP using a luciferase-based assay system. The results shown represent the amount of ATP in the treated groups as a percentage of the ATP present in the vehicle-treated group. Results are an average of three independent experiments. C, inhibition of ent1 does not block 6BT-mediated uptake into leukemic cells. HL-60 cells were treated with the indicated compounds with or without a low dose of 6BT (5 μmol/L) for 3 d, and the NBT reduction assay was performed as detailed in Fig. 2. Results are an average of three independent experiments.