Skip Navigation


Carcinogenesis Advance Access originally published online on July 13, 2006
Carcinogenesis 2007 28(2):267-279; doi:10.1093/carcin/bgl129
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
28/2/267    most recent
bgl129v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Maroni, P.
Right arrow Articles by Desiderio, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Maroni, P.
Right arrow Articles by Desiderio, M. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

HGF induces CXCR4 and CXCL12-mediated tumor invasion through Ets1 and NF-{kappa}B

Paola Maroni{dagger}, Paola Bendinelli{dagger}, Emanuela Matteucci and Maria Alfonsina Desiderio*

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

*To whom correspondence should be addressed. Tel: +39 025 031 5334; Fax: +39 025 031 5338; Email: a.desiderio{at}unimi.it

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-{kappa}B 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-{kappa}B was activated also by hypoxia and contributed, with HIF-1, to the increase in CXCR4 expression. The results suggest that Ets1, specifically activated by HGF, might cooperate with NF-{kappa}B activity to enhance the invasive/metastatic phenotype of breast carcinoma cells.

Abbreviations: EMSA, electrophoretic mobility shift assay; FBS, fetal bovine serum; HGF, hepatocyte growth factor; MMP1, metalloprotease-1

{dagger}These authors have contributed equally to this work.

Received February 23, 2006; revised May 29, 2006; accepted June 16, 2006.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol Cancer ResHome page
E. Matteucci, E. Ridolfi, P. Maroni, P. Bendinelli, and M. A. Desiderio
c-Src/Histone Deacetylase 3 Interaction Is Crucial for Hepatocyte Growth Factor Dependent Decrease of CXCR4 Expression in Highly Invasive Breast Tumor Cells
Mol. Cancer Res., August 1, 2007; 5(8): 833 - 845.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.