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. Author manuscript; available in PMC: 2015 Jan 28.
Published in final edited form as: Cancer Lett. 2014 Oct 18;356(2 0 0):656–668. doi: 10.1016/j.canlet.2014.10.015

Fig. 4.

Fig. 4

MK-1775 synergizes with LY2603618 in BxPC-3 cells. A, BxPC-3 cells were treated with variable concentrations of LY2603618 for 48 h and viable cells were determined by MTT assays. The data are presented as means ± standard errors from at least 3 independent experiments. B, BxPC-3 cells were treated with vehicle control, MK-1775 (MK), LY2603618 (LY) or MK-1775 plus LY2603618 for 48 h, stained with PI and subjected to flow cytometry analysis. C, protein extracts were subjected to Western blotting and probed with anti-PARP, -p-CHK1, -CHK1, -p-CDC25C, -p-CDK1, -CDK1, -p-CDK2, -CDK2, -γH2AX, or -β-actin antibody. D, BxPC-3 cells were treated with variable concentrations of MK-1775 with or without 0.25 μM, 0.5 μM or 1 μM LY2603618. Viable cells were measured by MTT assays and the data are presented as means ± standard errors from at least 3 independent experiments. E, standard isobologram analyses of antitumor interactions between MK-1775 and LY2603618 in BxPC-3 cells were performed.