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Inactive caspase 3 activates Akt in human leukemia cells susceptible or resistant to apoptosis induced by phorbol ester

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Affiliated Author(s)
박종욱권택규
Alternative Author(s)
Park, Jong WookKwon, Taeg Kyu
Journal Title
International Journal of Oncology
ISSN
1019-6439
Issued Date
2003
Abstract
Phorbol 12-myristate 13-acetate (PMA) is a protein kinase C (PKC) activator and tumor promoter that induces terminal differentiation in human myeloid leukemia cells. We undertook to characterize phorbol ester-activated PKC-mediated cell cycle arrest and apoptosis. In the present studies, we determined the effect of high intracellular levels of the anti-apoptosis Bcl-2 protein on caspase 3 activation and cyctochrome c release during phorbol ester 12-myristate 13-acetate (PMA)-induced apoptosis. For this, we used the U937 cells, Bcl-2 overexpressed U937 cells (U937/Bcl-2) and the PMA-resistant derivative cell line R-U937. The G1 arrest of U937 cells and U937/Bcl-2 cells induced by treatment with 20 nM PMA is associated with cyclin A down-regulation and accumulation of p21, cdks inhibitor. However, PMA had no effect on the levels of cyclin A expression and p21 expression under the same conditions of time and concentration of PMA in the R-U937 cells. Treatment with 20 nM PMA for 24 h produced morphological features of apoptosis and DNA fragmentation in U937 and U937/Bcl-2 cells, but not in R-U937 cells. This was associated with the caspase 3 activation and cyctochrome c release. R-U937 cells exhibited less cytochrome c release and sustained phosphorylation level of Akt during PMA-induced apoptosis. These findings indicate that R-U937 cells are resistant to PMA-induced apoptosis by a mechanism of the signaling defect in the activation of the caspase 3 that is involved in the execution of apoptosis.
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Jeong-Ok Hah et al. (2003). Inactive caspase 3 activates Akt in human leukemia cells susceptible or resistant to apoptosis induced by phorbol ester. International Journal of Oncology, 22(5), 1111–1116. doi: 10.3892/ijo.22.5.1111
Type
Article
ISSN
1019-6439
DOI
10.3892/ijo.22.5.1111
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35933
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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