scholarly journals PTHrP [67-86] regulates the expression of stress proteins in breast cancer cells inducing modifications in urokinase-plasminogen activator and MMP-1 expression

2003 ◽  
Vol 116 (12) ◽  
pp. 2421-2430 ◽  
Author(s):  
C. Luparello
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Plasminogen Activator ◽  
Breast Cancer Cells ◽  
Stress Proteins ◽  
Urokinase Plasminogen Activator

scholarly journals Rac1-MKK3-p38-MAPKAPK2 Pathway Promotes Urokinase Plasminogen Activator mRNA Stability in Invasive Breast Cancer Cells

2002 ◽  
Vol 277 (50) ◽  
pp. 48379-48385 ◽  
Author(s):  
Qiwei Han ◽  
Jay Leng ◽  
Dafang Bian ◽  
Chitladda Mahanivong ◽  
Kevin A. Carpenter ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Plasminogen Activator ◽  
Invasive Breast Cancer ◽  
Mrna Stability ◽  
Breast Cancer Cells ◽  
Urokinase Plasminogen Activator

scholarly journals Global Gene Expression Analysis Identifies PDEF Transcriptional Networks Regulating Cell Migration during Cancer Progression

2008 ◽  
Vol 19 (9) ◽  
pp. 3745-3757 ◽  
Author(s):  
David P. Turner ◽  
Victoria J. Findlay ◽  
A. Darby Kirven ◽  
Omar Moussa ◽  
Dennis K. Watson
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Differential Expression ◽  
Plasminogen Activator ◽  
Invasive Breast Cancer ◽  
Breast Cancer Cells ◽  
Urokinase Plasminogen Activator ◽  
Negative Regulator ◽  
Morphological Polarity

Prostate derived ETS factor (PDEF) is an ETS (epithelial-specific E26 transforming sequence) family member that has been identified as a potential tumor suppressor. In multiple invasive breast cancer cells, PDEF expression inhibits cell migration by preventing the acquisition of directional morphological polarity conferred by changes in cytoskeleton organization. In this study, microarray analysis was used to identify >200 human genes that displayed a common differential expression pattern in three invasive breast cancer cell lines after expression of exogenous PDEF protein. Gene ontology associations and data mining analysis identified focal adhesion, adherens junctions, cell adhesion, and actin cytoskeleton regulation as cell migration-associated interaction pathways significantly impacted by PDEF expression. Validation experiments confirmed the differential expression of four cytoskeleton-associated genes with known functional associations with these pathways: uPA, uPAR, LASP1, and VASP. Significantly, chromatin immunoprecipitation studies identified PDEF as a direct negative regulator of the metastasis-associated gene uPA and phenotypic rescue experiments demonstrate that exogenous urokinase plasminogen activator (uPA) expression can restore the migratory ability of invasive breast cancer cells expressing PDEF. Furthermore, immunofluorescence studies identify the subcellular relocalization of urokinase plasminogen activator receptor (uPAR), LIM and SH3 protein (LASP1), and vasodilator-stimulated protein (VASP) as a possible mechanism accounting for the loss of morphological polarity observed upon PDEF expression.

Exposure of MCF-7 Breast Cancer Cells to Electromagnetic Fields Up-Regulates the Plasminogen Activator System

2009 ◽  
Vol 19 (3) ◽  
pp. 334-338 ◽  
Author(s):  
Rainer Girgert ◽  
Günter Emons ◽  
Volker Hanf ◽  
Carsten Gründker
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Plasminogen Activator ◽  
Electromagnetic Fields ◽  
Breast Cancer Cells ◽  
Urokinase Plasminogen Activator ◽  
Plasminogen Activator System ◽  
Activator System ◽  
Mcf 7

Effects of electromagnetic fields (EMFs) on the incidence of breast cancer (BC) have been proposed by a number of epidemiological studies. The molecular mechanism of the impact of EMFs on cells is not yet clear, although changes in gene expression have been reported in various cellular systems. In this investigation, the interference of low-frequency EMFs with the plasminogen activator system was examined in BC cells.MCF-7 BC cells from 2 different sources were exposed to highly homogeneous 50-Hz EMFs. Changes in gene expression were analyzed by reverse transcriptase-polymerase chain reaction.In MCF-7 cells exposed to 1.2 μT EMF expression of the urokinase plasminogen activator gene and of plasminogen-activator inhibitor-1 was markedly increased. The expression of the receptor for urokinase plasminogen activator was only marginally increased in 1 of the 2 tested cell lines and expression of the tissue plasminogen activator was at least slightly down-regulated in BC cells exposed to EMFs.EMFs may be able to increase the metastatic potential of breast tumors. The use of our newly established exposure system for EMFs may allow us to study the signaling processes involved in the induction of a metastatic phenotype of breast cancer cells.

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