Figure 5
Vorinostat enhances inhibition of aurora kinases by MK-0457 in IM-sensitive and -resistant cells, including those bearing the T315I mutation. (A) K562 and LAMA84 cells were exposed to 5 to 100 nM MK with or without Vor (K562: 2 μM; LAMA84: 1.5 μM) for 48 hours (K562) or 24 hours (LAMA84). (B) IM-resistant K562-R cells were treated with 0.1 to 1 μM MK with or without 1.5 μM Vor for 48 hours. (C) Ba/F3 cells with wt or T315I Bcr/Abl were treated with 0.1 to 0.5 μM MK with or without 1.5 μM Vor for 48 hours. (A-C) After drug treatment, Western blot analysis was performed to monitor expression of total and phosphorylated (Ser 10) histone H3, as well as total aurora A and B. Each lane was loaded with 30 μg protein; blots were stripped and reprobed with antibodies to β-actin to ensure equal loading and transfer. Two additional studies yielded equivalent results.

Vorinostat enhances inhibition of aurora kinases by MK-0457 in IM-sensitive and -resistant cells, including those bearing the T315I mutation. (A) K562 and LAMA84 cells were exposed to 5 to 100 nM MK with or without Vor (K562: 2 μM; LAMA84: 1.5 μM) for 48 hours (K562) or 24 hours (LAMA84). (B) IM-resistant K562-R cells were treated with 0.1 to 1 μM MK with or without 1.5 μM Vor for 48 hours. (C) Ba/F3 cells with wt or T315I Bcr/Abl were treated with 0.1 to 0.5 μM MK with or without 1.5 μM Vor for 48 hours. (A-C) After drug treatment, Western blot analysis was performed to monitor expression of total and phosphorylated (Ser 10) histone H3, as well as total aurora A and B. Each lane was loaded with 30 μg protein; blots were stripped and reprobed with antibodies to β-actin to ensure equal loading and transfer. Two additional studies yielded equivalent results.

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