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. 2017 Jun 10;8(27):43678–43691. doi: 10.18632/oncotarget.18435

Figure 1. RB-dependent cell cycle inhibitory activity.

Figure 1

A. The indicated cell lines were treated with 1 µM palbociclib (PD) or 125 nM, 250 nM or 1 µM abemaciclib (LY). The relative BrdU incorporation was determined at 48 hours post-treatment. B. Immunoblots from the indicated cell lines developed with CRISP/Cas9 mediated deletion of RB. GAPDH is shown as a loading control. C. Representative BrdU (y-axis) vs. propidium iodide (x-axis) flow cytometry for RB-proficient and deficient models treated with palbociclib. D. The indicated cell lines were treated deleted for RB were treated with 1 µM palbociclib (PD) or 125 nM, 250 nM or 1 µM abemaciclib (LY). The relative BrdU incorporation was determined at 48 hours post-treatment. E. The indicated cell lines which are RB-deficient triple negative breast cancer models were were treated with 1 µM palbociclib (PD) or 125 nM, 250 nM or 1 µM abemaciclib (LY). The relative BrdU incorporation was determined at 48 hours post-treatment.