Reference : Transactivation of MCP-1/CCL2 by beta-catenin/TCF-4 in human breast cancer cells
Scientific journals : Article
Human health sciences : Oncology
http://hdl.handle.net/2268/11900
Transactivation of MCP-1/CCL2 by beta-catenin/TCF-4 in human breast cancer cells
English
Mestdagt, Mélanie [Université de Liège - ULg > Département des sciences cliniques > Labo de biologie des tumeurs et du développement >]
Polette, M. [> > > >]
Buttice, G. [> > > >]
Noël, Agnès mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie cellulaire et moléculaire appliquée à l'homme >]
Ueda, A. [> > > >]
Foidart, Jean-Michel mailto [Université de Liège - ULg > Département des sciences cliniques > Gynécologie - Obstétrique >]
Gilles, Christine mailto [Université de Liège - ULg > Département des sciences cliniques > Labo de biologie des tumeurs et du développement >]
1-Jan-2006
International Journal of Cancer = Journal International du Cancer
Wiley Liss, Inc.
118
1
35-42
Yes (verified by ORBi)
International
0020-7136
1097-0215
New York
NY
[en] MCP-1 ; beta-catenin ; breast cancer
[en] The loss of E-cadherin expression and the translocation of beta-catenin to the nucleus are frequently associated with the metastatic conversion of epithelial cells. In the nucleus, beta-catenin binds to the TCF/LEF-1 (T-cell factor/ lymphoid enhancer factor) transcription factor family resulting in the activation of several genes, some of them having important implications in tumour progression. In our study, we investigated the potential regulation of monocyte chemotactic protein-1 (MCP-1/CCL2) expression by the beta-catenin/TCF pathway. This CC-chemokine has been implicated in tumour progression events such as angiogenesis or tumour associated macrophage (TAM) infiltration. We thus demonstrated that MCP-1 expression correlates with the reorganization of the E-cadherin/beta-catenin complexes. Indeed, MCP-1 was expressed by invasive breast cancer cells (MDA-MB-231, BT549 and Hs578T), which do not express E-cadherin but was not produced by noninvasive breast cancer cell lines (MCF7 and T47D) expressing high level of E-cadherin. In addition, the MCP-1 promoter was activated in BT549 breast cancer cells transfected with beta-catenin and TCF-4 cDNAs. The MCP-1 mRNA level was similarly upregulated. Moreover, we showed that MCP-1 mRNA was downregulated after transfection with a siRNA against beta-catenin in both BT549 and Hs578T cells. Our results therefore identify MCP-1 as a target of the beta-catenin/TCF/LEF pathway in breast tumour cells, a regulation which could play a key role in breast tumour progression. (c) 2005 Wiley-Liss, Inc.
http://hdl.handle.net/2268/11900
10.1002/ijc.21291

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