| Item type |
文献 / Documents(1) |
| 公開日 |
2020-02-05 |
| アクセス権 |
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|
アクセス権 |
open access |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1111/j.1349-7006.1998.tb00481.x |
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|
言語 |
ja |
|
|
関連名称 |
10.1111/j.1349-7006.1998.tb00481.x |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Putrescine‐stimulated Intracellular Ca2+ Release for Invasiveness of Rat Ascites Hepatoma Cells |
|
言語 |
en |
| タイトル別表記 |
|
|
その他のタイトル |
Putrescine-dependent Tumor Invasion |
|
言語 |
en |
| 著者 |
アシダ, ヨシユキ
ウエノ, アケミチ
ミワ, ヨシヒロ
三好, 圭子
イノウエ, ヒデオ
|
| 抄録 |
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|
内容記述タイプ |
Abstract |
|
内容記述 |
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. |
|
言語 |
en |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Putrescine |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Tumor invasion |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Difluoromethylornithine |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Ryanodine |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Thapsigargin |
| 書誌情報 |
en : Japanese Journal of Cancer Research
巻 89,
号 1,
p. 67-75,
発行日 1998-01
|
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA00690844 |
| 出版者 |
|
|
出版者 |
Japanese Cancer Association |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
John Wiley & Sons |
|
言語 |
en |
| EID |
|
|
識別子 |
286332 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
jjcr_89_1_67.pdf (118 KB)
