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Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro
Author(s) -
Akao Yukihiro,
Nakagawa Yoshihito,
Akiyama Kiyotaka
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00841-8
Subject(s) - arsenic trioxide , neuroblastoma , apoptosis , dna fragmentation , acute promyelocytic leukemia , cancer research , retinoic acid , cell culture , chemistry , programmed cell death , caspase 3 , microbiology and biotechnology , medicine , biology , biochemistry , genetics
Arsenic trioxide (As 2 O 3 ) induces clinical remission in acute promyelocytic leukemia, even in all‐ trans retinoic acid‐refractory cases, with minimal toxicity at low (1–2 μM) concentration. We exposed various neuroblastoma cell lines to As 2 O 3 at a concentration of 2 μM: as a result, seven of 10 neuroblastoma cell lines underwent apoptosis characterized by morphological changes and nucleosomal DNA fragmentation. As 2 O 3 ‐induced apoptosis in neuroblastoma cells was shown to occur through the activation of caspase 3, as judged from Western blot analysis and apoptosis inhibition assay. It seemed that the sensitivity of neuroblastoma cells to As 2 O 3 was inversely proportional to their intracellular level of reduced glutathione. Taken together these results indicate that As 2 O 3 would be a candidate as a therapeutic agent for treatment of neuroblastoma, which is a solid tumor, not only by systemic therapy but also by local therapy.