Transforming growth factor β1 alters calcium mobilizing properties and endogenous ATP release in A549 cells: possible implications for cell migration
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- Miki Kenji
- Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Japan
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- Tanaka Hiromitsu
- Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Japan
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- Nagai Yoko
- Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Japan
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- Kimura Chiwaka
- Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Japan
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- Oike Masahiro
- Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Japan
書誌事項
- タイトル別名
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- Transforming Growth Factor .BETA.1 Alters Calcium Mobilizing Properties and Endogenous ATP Release in A549 Cells: Possible Implications for Cell Migration
- Transforming growth factor v 1 alters calcium mobilizing properties and endogenous ATP release in A549 cells possible implications for cell migration
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We examined the effects of transforming growth factor β1 (TGFβ1) on cellular functions in human lung cancer cell line A549. Treatment of A549 cells with 1 ng/ml TGFβ1 for more than 3 days altered their morphology from an epithelial cobblestone-like appearance to a fibroblast-like one, reduced the expression of E-cadherin mRNA and protein, and induced the formation of F-actin fibers. These hallmarks indicate that TGFβ1 induced the epithelial–mesenchymal transition in A549 cells. Migration of TGFβ1-treated A549 cells, which was quantified by the wound-healing assay, was markedly accelerated by 3 μM ATPγS, a non-hydrolyzable ATP analogue. ATPγS-induced migration of TGFβ1-treated A549 cells was reversed by the P2 antagonist suramin. In contrast, migration of control A549 cells was not altered by ATPγS. TGFβ1-treated A549 cells showed an augmentation of ATP-induced Ca2+ transients, thapsigargin-induced Ca2+ transients, and store-operated Ca2+ entry compared with those in control cells. Basal level of the extracellular ATP concentration was significantly lower in TGFβ1-treated A549 cells than in control cells. We conclude from these results that TGFβ1 augments ATP-induced Ca2+ mobilization, which leads to the acceleration of migration, in A549 cells but, it markedly reduces endogenous ATP release. This implies that the actions of ATP would become a novel therapeutic target for inhibiting cancer cell migration.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 113 (4), 387-394, 2010
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205179585536
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- NII論文ID
- 130000301216
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10790676
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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