Fig. 6

ABE and JQ1 were synergetic in vivo through inducing cell cycle arrest and cellular senescence. A Schemes for the in vivo experimental procedures to evaluate anticancer activities of ABE and JQ1. B, C Combination of ABE and JQ1 treatment improved the antitumor efficacy of Abemaciclib agents in vivo in the HGC27 tumor models. HGC27 cells (5 × 106/mouse) were subcutaneously injected into Balb/c- nu mice. Tumor-bearing mice received solvent control, abemaciclib (50 mg kg − 1 body weight) by oral, JQ1 (35 mg kg − 1 body weight) by intraperitoneal injection. Tumor volumes shown in (C) were measured and presented as mean ± SEM (n = 8 mice/group). Representative images of the xenograft tumors obtained from the indicated groups at the endpoint of the experiments (day 27) are shown in (B). D Histogram results showing the mean ± SEM of the tumor weights from the indicated groups at the endpoint of the experiments. E Line chart showing the mouse weight from the indicated groups. F Representative images for indicated assays in the end of study tumors showing the immunohistological evaluation of cellular proliferation by Ki-67 staining, the bottom panel shows the RB phosphorylation, each for the treatment cohort as labeled. Scale bar = 50 μm. G Statistics data represent mean ± SEM (n = 10) of Ki67 and pRB for each group. H Western blotting images showing the pRB in tumor lysates derived from the indicted treatment cohort. GAPDH was used as a loading control. I Statistics data represent mean ± SEM (n = 3) of Phospho-Rb (Ser807/811) protein level for each group