Modulation of reactive oxygen species by antioxidants in chronic myeloid leukemia cells enhances imatinib sensitivity through survivin downregulation.

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.