ID | 114224 |
Title Alternative | Putrescine-dependent Tumor Invasion
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Author |
Ashida, Yoshiyuki
Tokushima University|Hiroshima University
Ueno, Akemichi
Tokushima University
Miwa, Yoshihiro
Tokushima University
Miyoshi, Keiko
Tokushima University
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Inoue, Hideo
Tokushima University
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Keywords | Putrescine
Tumor invasion
Difluoromethylornithine
Ryanodine
Thapsigargin
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Content Type |
Journal Article
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Description | Our previous study showed that treatment of highly invasive rat ascites hepatoma (LC-AH) cells with α-difluoromethylornithine (DFMO), an inhibitor of ornithine decarboxylase, decreased both their intracellular level of putrescine and their in vitro invasion of a monolayer of calf pulmonary arterial endothelial (CPAE) cells, and that both these decreases were completely reversed by exogenous putrescine, but not spermidine or spermine. Here we show that all adhering control (DFMO-untreated) cells migrated beneath CPAE monolayer with morphological change from round to cauliflower-shaped cells (migratory cells). DFMO treatment increased the number of cells that remained round without migration (nonmigratory cells). Exogenous putrescine, but not spermidine or spermine, induced transformation of all nonmigratory cells to migratory cells with a concomitant increase in their intracellular Ca2+ level, [Ca2+]i. The putrescine-induced increase in their [Ca2+]i preceded their transformation and these effects of putrescine were not affected by antagonists of the voltage-gated Ca2+ channel, but were completely suppressed by ryanodine, which also suppressed the invasiveness of the control cells. The DFMO-induced decreases in both [Ca2+]i and the invasiveness of the cells were restored by thapsigargin, which elevated [Ca2+]i by inhibiting endoplasmic Ca2+-ATPase, indicating that thapsigargin mimics the effects of putrescine. These results support the idea that putrescine is a cofactor for Ca2+ release through the Ca2+ channel in the endoplasmic reticulum that is inhibited by ryanodine, this release being initiated by cell adhesion and being a prerequisite for tumor cell invasion.
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Journal Title |
Japanese Journal of Cancer Research
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NCID | AA00690844
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Publisher | Japanese Cancer Association|John Wiley & Sons
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Volume | 89
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Issue | 1
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Start Page | 67
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End Page | 75
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Published Date | 1998-01
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EDB ID | |
DOI (Published Version) | |
URL ( Publisher's Version ) | |
FullText File | |
language |
eng
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TextVersion |
Publisher
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departments |
Oral Sciences
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