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Phospholipase D Prevents Etoposide-Induced Apoptosis by Inhibiting the Expression of Early Growth Response-1 and Phosphatase and Tensin Homologue Deleted on Chromosome 10

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Affiliated Author(s)
권택규
Alternative Author(s)
Kwon, Taeg Kyu
Journal Title
Cancer Research
ISSN
0008-5472
Issued Date
2006
Abstract
Phospholipase D (PLD) has emerged as a critical regulator of
cell proliferation and survival signaling. We show for the first
time that elevated expression of PLD isozymes attenuates
expression of the tumor suppressors early growth response-1
(Egr-1) and the phosphatase and tensin homologue deleted on
chromosome 10 (PTEN) tumor suppressor and apoptosis
during etoposide treatment. When formation of phosphatidic
acid was inhibited by overexpression of catalytically inactive
PLD during etoposide treatment, expression of Egr-1 and PTEN
and the apoptotic effect of etoposide were not inhibited. This
suggests that PLD inhibits expression of these tumor suppressors
and inhibits apoptosis. Deletion of a specific Egr-1-binding
site present in the PTEN promoter blocked etoposide-induced
PTEN activity and elevated expression of PLD decreased the
sensitivity to apoptosis induced by ectopic expression of Egr-1.
Etoposide-induced activation of Akt was potentiated by overexpression
of PLD and PLD-stimulated suppression of Egr-1
was blocked by inhibition of phosphatidylinositol 3-kinase/Akt
survival pathway at the both transcriptional and posttranscriptional
levels. These results show that survival signals
generated by PLD attenuate expression of Egr-1 by activation of
phosphatidylinositol 3-kinase signaling pathway and induction
of PTEN by Egr-1, which confers resistance to apoptosis. (Cancer
Res 2006; 66(2): 784-93)
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Joommo Kim et al. (2006). Phospholipase D Prevents Etoposide-Induced Apoptosis by Inhibiting the Expression of Early Growth Response-1 and Phosphatase and Tensin Homologue Deleted on Chromosome 10. Cancer Research, 66(2), 784–793. doi: 10.1158/0008-5472.CAN-05-1316
Type
Article
ISSN
0008-5472
DOI
10.1158/0008-5472.CAN-05-1316
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34814
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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