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Peroxiredoxin 3 Has Important Roles on Arsenic Trioxide Induced Apoptosis in Human Acute Promyelocytic Leukemia Cell Line via Hyperoxidation of Mitochondrial Specific Reactive Oxygen Species

 Yeung-Chul Mun  ;  Jee Young Ahn  ;  Eun Sun Yoo  ;  Kyoung Eun Lee  ;  Eun Mi Nam  ;  Jungwon Huh  ;  Hyun Ae Woo  ;  Sue Goo Rhee  ;  Chu Myong Seong 
 MOLECULES AND CELLS, Vol.43(9) : 813-820, 2020-09 
Journal Title
Issue Date
Antineoplastic Agents / pharmacology* ; Apoptosis / drug effects ; Arsenic Trioxide / pharmacology* ; Cell Line, Tumor ; Humans ; Leukemia, Promyelocytic, Acute / drug therapy* ; Leukemia, Promyelocytic, Acute / metabolism ; Leukemia, Promyelocytic, Acute / pathology ; Mitochondria / metabolism* ; Peroxiredoxin III / metabolism* ; Reactive Oxygen Species / metabolism ; Transfection
acute promyelocytic leukemia ; arsenic trioxide ; peroxiredoxin 3
NB4 cell, the human acute promyelocytic leukemia (APL) cell line, was treated with various concentrations of arsenic trioxide (ATO) to induce apoptosis, measured by staining with 7-amino-actinomycin D (7-AAD) by flow cytometry. 2', 7'-dichlorodihydro-fluorescein-diacetate (DCF-DA) and MitoSOXTM Red mitochondrial superoxide indicator were used to detect intracellular and mitochondrial reactive oxygen species (ROS). The steady-state level of SO2 (Cysteine sulfinic acid, Cys-SO2H) form for peroxiredoxin 3 (PRX3) was measured by a western blot. To evaluate the effect of sulfiredoxin 1 depletion, NB4 cells were transfected with small interfering RNA and analyzed for their influence on ROS, redox enzymes, and apoptosis. The mitochondrial ROS of NB4 cells significantly increased after ATO treatment. NB4 cell apoptosis after ATO treatment increased in a time-dependent manner. Increased SO2 form and dimeric PRX3 were observed as a hyperoxidation reaction in NB4 cells post-ATO treatment, in concordance with mitochondrial ROS accumulation. Sulfiredoxin 1 expression is downregulated by small interfering RNA transfection, which potentiated mitochondrial ROS generation and cell growth arrest in ATO-treated NB4 cells. Our results indicate that ATO-induced ROS generation in APL cell mitochondria is attributable to PRX3 hyperoxidation as well as dimerized PRX3 accumulation, subsequently triggering apoptosis. The downregulation of sulfiredoxin 1 could amplify apoptosis in ATO-treated APL cells.
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1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Rhee, Sue Goo(이서구)
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