Key result
Inhibiting catalase activity significantly enhanced imatinib-induced apoptosis (P<0.05) by diminishing survivin expression in K562 chronic myeloid leukemia cells.
p-value: p=<0.05
Inhibiting catalase activity enhances imatinib-induced apoptosis in chronic myeloid leukemia cells by downregulating survivin.
Catalase inhibition may potentiate imatinib in CML; hypothesis-generating from cell-line data and requires clinical validation.
Survivin, a member of the inhibitor of apoptosis protein family and a target for new drugs, is modulated by reactive oxygen species in several types of neoplasms including leukemias. The aim of this study is to find mechanisms to enhance sensitivity to imatinib in imatinib-responsive cells. In this study, we demonstrated through fluorescein isothiocyanate-labeled annexin V for apoptotic cells detection and western blotting that by inhibiting catalase activity, imatinib apoptosis induction was significantly enhanced (P<0.05) through diminishing survivin expression in K562 cells. These findings might be of clinical relevance and might help improve the chemotherapeutic use of imatinib mesylate.
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Kwee et al. (2008) studied Chronic myeloid leukemia. Inhibition of catalase activity combined with imatinib was evaluated on Apoptosis induction and survivin expression (p=<0.05). Inhibiting catalase activity significantly enhanced imatinib-induced apoptosis (P<0.05) by diminishing survivin expression in K562 chronic myeloid leukemia cells.
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