Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/38369
標題: Effects of Genistein on beta-Catenin Signaling and Subcellular Distribution of Actin-Binding Proteins in Human Umbilical CD105-Positive Stromal Cells
作者: Shieh, D.B.
劉英明
Li, R.Y.
Lia, J.M.
Chen, G.D.
Liou, Y.M.
關鍵字: mesenchymal stem-cells
breast-cancer cells
nonmuscle caldesmon
telomerase activity
atp hydrolysis
mouse oocytes
cross-talk
cyclin
d1
in-vitro
tropomyosin
期刊/報告no:: Journal of Cellular Physiology, Volume 223, Issue 2, Page(s) 423-434.
摘要: This study was performed to define the roles of actin-binding proteins in the regulation of actin filament assembly associated with cellular signal transduction pathways in stromal cell proliferation. Genistein, a tyrosine protein kinase inhibitor, decreased the intracellular Ca(2+) and attenuated cell proliferation and DNA synthesis through the beta-catenin and cyclin D1 pathway in human umbilical CD105-positive cells. Immunoprecipitation studies using anti-beta-actin antibody revealed that several actin-binding proteins implicated in cells include formin-2 (FMN-2), caldesmon (CaD), tropomyosin (Tm), and profilin. Protein levels of these proteins in whole cell lysates were not significantly changed by genistein. Three Tm isoforms, Tm-1, Tm-2, and Tm-4, were found to be present in cells. Genistein caused a reduction in levels of mRNAs coding for Tm-1 and Tm-4, but had no significant effect on Tm-2 mRNA levels. Immunofluorescence confocal scanning microscopy indicated that changes in the subcellular distribution of Tm and CaD, in which the diffuse cytosolic staining was shifted to show colocalization with actin stress fibers. In contrast, genistein-induced accumulation of FMN-2 and profilin in the pen-nuclear area. Silencing of FMN-2 by small interfering RNA resulted in increases of intracellular Ca(2+) and rendered genistein resistance in decreasing intracellular Ca(2+) in cells. These results provide the novel findings that genistein acts by modulating the cellular distribution of actin-binding proteins in association with alterations of cellular signal transduction pathways in human stromal cell proliferation. J. Cell. Physiol. 223: 423-434, 2010. (C) 2010 Wiley-Liss, Inc.
URI: http://hdl.handle.net/11455/38369
ISSN: 0021-9541
文章連結: http://dx.doi.org/10.1002/jcp.22051
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