Figure 7
BafA1 suppresses HCC growth in mouse tumor xenografts and is enhanced by JNK inhibition.
Six week old female nude mice bearing BEL7402 and HepG2 tumors were randomized into four groups: (a) vehicle-treated, (b) SP600125 (intraperitoneal (ip) three times per week), (c) BafA1 (10 mg/kg) via intratumoral administration three times per week, (d) BafA1 treatment in combination with SP600125, the inhibitor (SP600125) was administered one day prior to treatment with BafA1. (A) Tumor volumes were measured at 5-day intervals for 50 days and expressed as the mean ± SD (n = 10) in tumor volume-time curves. Differences in tumor regression were significant between BafA1-treated mice and vehicle control groups and in mice receiving combined treatments and treatment alone (BafA1 or drugs alone) (*p < 0.05; **p < 0.01; ***P < 0.001). No statistical significance was observed between mice receivsing single treatments alone and vehicle controls (B) Five weeks after treatment, tumor tissue samples from each treatments group were subjected to either hematoxylin-eosin (H&E) staining (the upper panels, tumor necrosis indicated by white arrows) or TUNEL assay (the lower panels, arrowheads indicate brown 3,3′-diaminobenzidine chromogen in the cell nuclei of apoptotic cells), (BafA1 means Bafilomycin A1).
