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학술저널
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문영철 (이화여자대학교) Jee Young Ahn (Ewha Womans University College of Medicine) Eun-Sun Yoo (Ewha Womans University) Kyoung Eun Lee (Department of Hematology-Oncology Ewha Woman's University School of Medicine) Eunmi Nam (Ewha Women's University) Jungwon Huh (Ewha Womans University) Hyun Ae Woo (Ewha Womans University) Sue Goo Rhee (Yonsei University College of Medicine) 성주명 (이화여자대학교)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제43권 제9호
발행연도
2020.1
수록면
813 - 820 (8page)

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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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