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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

Title
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
Authors
Mun Y.-C.Ahn J.Y.Yoo E.S.Lee K.E.Nam E.M.Huh J.Woo H.A.Rhee S.G.Seong C.M.
Ewha Authors
성주명유은선허정원이경은문영철남은미우현애
SCOPUS Author ID
성주명scopus; 유은선scopus; 허정원scopus; 이경은scopus; 문영철scopus; 남은미scopus; 우현애scopus
Issue Date
2020
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
Molecules and Cells vol. 43, no. 9, pp. 813 - 820
Keywords
Acute promyelocytic leukemiaArsenic trioxidePeroxiredoxin 3
Publisher
Korean Society for Molecular and Cellular Biology
Indexed
SCIE; SCOPUS; KCI WOS scopus
Document Type
Article
Abstract
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 MitoSOX™ 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–SO2 H) 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. © The Korean Society for Molecular and Cellular Biology. All rights reserved.
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DOI
10.14348/molcells.2020.2234
Appears in Collections:
의과대학 > 의학과 > Journal papers
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