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Carcinogenesis Advance Access published online on July 13, 2006
Carcinogenesis, doi:10.1093/carcin/bgl129
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received February 23, 2006
Revised May 29, 2006
Accepted June 16, 2006

CANCER BIOLOGY

HGF differs from hypoxia in activating Ets1 for CXCR4 expression and invasiveness of MCF-7 breast cancer cells

Paola Maroni 1 1, Paola Bendinelli 1 1, Emanuela Matteucci 1, and Maria Alfonsina Desiderio 1 *

1 Institute of General Pathology, University of Milan, via Luigi Mangiagalli, 31-20133 Milan, Italy

* To whom correspondence should be addressed.
Maria Alfonsina Desiderio, E-mail: a.desiderio{at}unimi.it


  Abstract

CXCR4 is a chemokine receptor probably involved in the homing of metastatic breast cancer, and its expression is modulated by tumor environmental stimuli such as hepatocyte growth factor (HGF) and hypoxia. Here we demonstrate that, depending on the stimulus, different transcription factors can cooperate in enhancing CXCR4 transcription in MCF-7 breast cancer cell line. In HGF-treated MCF-7 cells, the DNA binding of Ets1 activated by MAPK1/ERK1/2 transduction pathway as well as the DNA binding of NF-kB played a critical role in CXCR4 transcription and protein induction. Under HGF stimulation, the blockade of these transcription factors by dominant negatives and inhibitors prevented the expression of CXCR4 receptor, the activity of a gene reporter driven by CXCR4 promoter sequence and the chemoinvasion toward the CXCL12 ligand. NF-kB was activated also by hypoxia and participated with HIF-1 to the increase in CXCR4 expression. The results suggest that Ets1, specifically activated by HGF, might cooperate with NF-kB activity to enhance the invasive/metastatic phenotype of breast carcinoma cells.

1These Authors equally contributed to the work.
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 Mol Cancer ResHome page
E. Matteucci, E. Ridolfi, P. Maroni, P. Bendinelli, and M. A. Desiderio
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[Abstract] [Full Text] [PDF]


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