RB inhibits growth of RM-1 homografts in C57BL/6 mice and triggers apoptosis.

<p>(A) RB and AKBA concentration-dependently inhibited the Ser-536 phosphorylation of p65 in RM-1 cells. GAPDH served as the loading control. (B) RB (25 mg/kg) reduced the tumor volumes in RM-1-bearing C57BL/6 mice versus the control group, AKBA serving as positive control. 0.2×10⁶ RM-1 cells were s.c. injected into the dorsal region of right side, and after 7 days, the animals were treated intraperitoneally with RB (25 mg/kg), AKBA (25 mg/kg) or medium alone (control) once daily for 18 days, as described in <i>Materials and Methods</i>, n = 6 per group; mean ± SD; p<0.05 (*), p<0.01 (**), p<0.001(***) versus medium control group, respectively. (C) Representative tumors from the three groups are shown. (D) H&E and TUNEL-dependent staining of RM-1 tumor tissue sections. (Scale bar, 100 μm). (E) Western blot analysis of p–p65, PARP, Bax, Bcl-2, and Bcl-x_L expression in 2 tumor tissue samples treated with medium, 4 samples with RB and 2 samples with AKBA. (F) Immunofluorescence for p–p65 analysis of tumor tissues. (Scale bar, 100 μm).