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031 Journal of Nara Medical Association >
Vol.54 No.2 >
Please use this identifier to cite or link to this item:
http://hdl.handle.net/10564/103
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| Title: | Molecular Mechanism of Arsenic Trioxide-Induced Apoptosis in HL-60 and Cell Lines |
| Authors: | Zhu, Jiebin
Nakamura, Shinobu |
| Keywords: | arsenic trioxide
HL-60
RL
apoptosis
CD95/CD95L pathway |
| Issue Date: | 30-Apr-2003 |
| Publisher: | 奈良医学会 |
| Citation: | Journal of Nara Medical Association Vol.54 No.2 p.113-123 |
| Abstract: | Recently, it has been reported that arsenic trioxide (As2 O3) is an effective
anticancer agent for acute promyelocytic leukemia (APL). In the present study, we
examined the anticancer effects of As2 O3 at low concentration (0.25～2.OμM) on two hunan
leukemia/lymphoma cell lines, HL-60 and RL, in vitro. We found that As2 O3 inhibited the
growth of HL-60 and RL similar to the reported APL cell line, NB4. Typical apoptosis
was observed in morphologlcal study and DNA fragmentation assay, as well as a cell
cycle arrest at subG1. To address the mechanism of As2 03-induced apoptosis, we also
examined the effect of As2 O3 on the CD95/CD95L pathway and bcl-2 protein expression.
The results showed that the CD95/CD95L expressions were upregulated; meanwhile,
caspase 8 and caspase 3 were activated. However, the bcl-2 protein expression was
downregulated. Using anti-CD95 monoclonal antibody to block the CD95 pathway,
As2 O3 - induced apoptosis was ameliorated. These data suggest that in HL-60 and RL cell
lines the CD95/CD95L pathway and downregulation of bc1-2 protein expression are
invoIved in As2 O3-induced apoptosis. |
| URI: | http://hdl.handle.net/10564/103 |
| ISSN: | 13450069 |
| Appears in Collections: | Vol.54 No.2
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Files in This Item:
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| 113-123p.Molecular Mechanism of Arsenic Trioxide-Induced Apoptosis in HL-60 and Cell Lines(Jiebin ZHU and Shinobu NAKAMURA).pdf | | 742Kb | Adobe PDF | View/Open |
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