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ORIGINAL ARTICLE
Year : 2010  |  Volume : 3  |  Issue : 1  |  Page : 62-71

The NF-κB inhibitor iκbα negates colon cancer cell migration, invasion, proliferation and tumor growth


1 Department of Pharmacology & Therapeutics, Faculty of Medicine & Health Sciences, UAE University, P. O Box 17666, Al Ain, United Arab Emirates; INSERM U 673 and U938, Molecular and Clinical Oncology of Solid Tumors; University Pierre et Marie Curie Paris VI, Hôpital Saint-Antoine, 75571 Paris Cedex 12, France
2 Department of Biology, UAE University, P. O. Box: 17551, Al Ain, United Arab Emirates; Institut Albert Bonniot, INSERM U823, University Joseph Fourier, Grenoble 1, Site Santé, 38042, Grenoble, Cedex 6, France
3 Department of Pathology, Faculty of Medicine & Health Sciences, UAE University, P. O Box 17666, Al Ain, United Arab Emirates
4 Department of Pharmacology & Therapeutics, Faculty of Medicine & Health Sciences, UAE University, P. O Box 17666, Al Ain, United Arab Emirates
5 Laboratory of Experimental Cancer Research, University Hospital, De Pintelaan 185, B-9000 Gent, Belgium
6 INSERM U 673 and U938, Molecular and Clinical Oncology of Solid Tumors; University Pierre et Marie Curie Paris VI, Hôpital Saint-Antoine, 75571 Paris Cedex 12, France

Correspondence Address:
Samir Attoub
Department of Pharmacology and Therapeutics, Faculty of Medicine & Health Sciences, UAE University, P.O. Box 17666, Al Ain

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Source of Support: None, Conflict of Interest: None


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It is now well accepted that the NF-κB pathways are involved in inflammatory diseases, cancer development and progression in human solid tumors. The NF-κB signaling element IκBα was shown to inactivates NF-κB activity through sequestration of this transcription factor in the cytoplasm. In the present study, we investigated the impact of the IκBα on the invasive growth of human colon cancer cells HCT8/S11 stably transfected by this endogenous NF-κB inhibitor. We report that IκBα ectopic expression inhibited NF-κB promoter activity induced by the Y527Fsrc oncogene, and reduced HCT8/S11 cell migration in wound healing assays. Our data show that IκBα abrogated collagen type I invasion induced by the trefoil factors TFF1 and TFF3, but was ineffective on the invasive phenotype determined by leptin. Moreover, IκBα reduced HCT8/S11 cell proliferation in vitro and the growth of their corresponding tumor xenografts established in the athymic mice. Taken together our data demonstrated that the intrinsic NF-κB inhibitor IκBα negates several transforming functions in human colon cancer cells. Our data provide the rationale for further preclinical and clinical studies based on therapeutic interventions targeting NF-κB pathway.


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