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Title: Density- and serum-dependent regulation of the Reck tumor suppressor in mouse embryo fibroblasts.
Authors: Hatta, Mamiko
Matsuzaki, Tomoko  kyouindb  KAKEN_id
Morioka, Yoko
Yoshida, Yoko  kyouindb  KAKEN_id
Noda, Makoto  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 野田, 亮
八田, 真美子
Keywords: Mmp2
Issue Date: Dec-2009
Publisher: Elsevier
Journal title: Cellular signalling
Volume: 21
Issue: 12
Start page: 1885
End page: 1893
Abstract: Reck is a membrane-anchored glycoprotein identified as a transformation suppressor. Accumulating evidence indicates that Reck negatively regulates a wide spectrum of matrix metalloproteinases and is commonly down-regulated in a variety of malignant solid tumors. Physiological cues that regulate Reck expression, however, remained unknown. In this study, we found that Reck expression was up-regulated at high cell density, low serum, or after treatment with some kinase inhibitors, such as PP2 (Src inhibitor), LY294002 (PI3-kinase inhibitor), and PF573228 (FAK inhibitor), in mouse embryo fibroblasts. Curve fitting indicated that the levels of Reck protein and Reck mRNA are quadratic in the cell density. Other factors, including serum, extracellular matrix components (type I collagen and fibronectin), the kinase inhibitors, and some of their oncogenic targets (v-Src and PIK3CA mutants), modify the shape of the quadratic curve. Comparison of these modifications implicated Src in Reck down-regulation under sparse conditions, PI3-kinase in serum-induced Reck down-regulation, and FAK in Reck down-regulation at high cell density. Fibronectin and type I collagen down-regulated Reck, supporting the role of integrin-FAK signaling in Reck down-regulation at high cell density. Our study has revealed multiple signaling pathways impinging on Reck in cultured mouse embryo fibroblasts and sets a foundation for future studies to find effective Reck inducers of potential value in cancer therapy.
Rights: © 2009 Elsevier B.V.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
DOI(Published Version): 10.1016/j.cellsig.2009.08.005
PubMed ID: 19720143
Appears in Collections:Journal Articles

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