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- W2260506987 abstract "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." @default.
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- W2260506987 date "2010-01-01" @default.
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- W2260506987 title "The NF-kB Inhibitor IkBa Negates Colon Cancer Cell Migration, Invasion, Proliferation and Tumor Growth" @default.
- W2260506987 doi "https://doi.org/10.2174/1996327001003010062" @default.
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