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. 2020 Aug 25;14(10):2533–2545. doi: 10.1002/1878-0261.12775

Fig. 2.

Fig. 2

The cAMP‐hydrolyzing PDE3 inhibitor cilostazol phenocopies dipyridamole to potentiate statin‐induced cancer cell death. (A) Schematic representation of the reported targets of dipyridamole and additional compounds that target these proteins. ENT, equilibrative nucleoside transporter; GLUT, glucose transporter; PDE, phosphodiesterase; PKA, protein kinase A. (B) OCI‐AML‐2, OCI‐AML‐3, and KMS11 cells were treated with atorvastatin (4, 2 and 4 µm for OCI‐AML‐2, OCI‐AML‐3, and KMS11 cells, respectively) ± a glucose uptake inhibitor (fasentin; 12.5, 6.3, and 12.5 µm for OCI‐AML‐2, OCI‐AML‐3, and KMS11 cells, respectively), ENT inhibitor (NBMPR; 20 µm), cGMP‐hydrolyzing PDE5 inhibitor (MBMQ; 10 µm), or cAMP‐hydrolyzing PDE3 inhibitor (cilostazol; 25, 12.5, and 25 µm for OCI‐AML‐2, OCI‐AML‐3, and KMS11 cells, respectively). After 48 h, cell viability was evaluated by MTT assays. Data are represented as the mean + SD. *P < 0.05 (one‐way ANOVA with Tukey's multiple comparisons test, where the indicated groups were compared to the other groups of that cell line). # P < 0.05 (one‐way ANOVA with Tukey's multiple comparisons test, comparing the two indicated groups).