期刊
MOLECULAR CANCER RESEARCH
卷 10, 期 1, 页码 121-132出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-11-0180
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资金
- Fonds National de la Recherche Scientifique (F.N.R.S., Belgium)
- Fondation contre le Cancer (Belgium)
- PHC-Tournesol (Belgium)
- Fonds de la Recherche Scientifique Medicale
- Fonds speciaux de la Recherche (University of Liege)
- Centre Anticancereux pres l'Universite de Liege
- Fonds Leon Fredericq (University of Liege)
- Region Champagne-Ardenne
- Ligue Contre le Cancer
- Lions Club of Soissons
- European Framework Programme 7 MICRO-ENVIMET
Accumulating data now suggest that ZO-1, once delocalized from tight junctions, could be implicated in the regulation of tumor-promoting genes. Because of their major implication in different steps of tumor progression, we investigated here the influence of ZO-1 on chemokines expression in breast cancer cells. Using GeneArray analysis to compare chemokine mRNA expression in breast tumor cells transfected with a siRNA against ZO-1, we identified CXCL-8IL-8 as a major potential target of ZO-1 signaling, being strongly downregulated following ZO-1 siRNA transfection. Examining further the relationship between ZO-1 and interleukin-8 (CXCL8/IL-8), we first showed that CXCL8/IL-8 expression correlates with a relocalization of ZO-1 in several breast cancer cell lines. Moreover, CXCL8/IL-8 is downregulated in invasive BT549 cells transfected with three different ZO-1 siRNA and overexpressed in noninvasive BT20 and SKBR3 cells transfected with vectors expressing ZO-1. We also provide evidence for an activation of the CXCL8/IL-8 promoter by ZO-1. Finally, we show that the regulation of CXCL 8/IL-8 by ZO-1 is independent of the beta-catenin pathway. Our results thus clearly show an implication of ZO-1 in CXCL8/IL-8 regulation. Because of the major implications of CXCL8/IL-8 in tumor invasion, such a regulation could play an important role in breast cancer progression. Mol Cancer Res; 10(1); 121-32. (C) 2011 AACR.
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