This study involves the antitumor potential of 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG) to induce apoptosis and enhance antitumor activity of imatinib in K562 cells. Though PGG was reported to have antitumor activities in breast, prostate, kidney, liver cancers and HL-60 leukemia cells, there is no report on synergistic antitumor effect of PGG with imatinib until now. In the present study, PGG significantly enhanced the cytotoxicty and cleavage of poly (ADP-ribose) polymerase (PARP) in imatinib induced chronic myeloid leukemia K562 cells. Furthermore, oral administration of PGG or imatinib significantly inhibited the growth of K562 cells inoculated in Balb/c athymic nude mice and also immunohistochemistry revealed decreased expression of Ki67 (proliferation), CD34 (blood density) and death domain-associated protein (DAXX) and increased terminal deoxynucleotide transferasemediated dUTPnick end labeling (TUNEL) positive cells as one of the apoptotic feature in tumor sections of K562 mouse xenograft model comparable to imatinib treated group. Overall, our findings suggest the potency of PGG to induce apoptosis and enhance antitumor activity of imatinib inK562 cells.
Key words: Chronic myeloid leukemia, apoptosis, 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG), imatinib.
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