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      NF-κB p50 promotes tumor cell invasion through negative regulation of invasion suppressor gene CRMP-1 in human lung adenocarcinoma cells

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      Biochemical and Biophysical Research Communications
      Elsevier BV

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          Abstract

          Lung adenocarcinoma Cl1-5 cells were selected from parental Cl1-0 cells based on their high metastatic potential. In a previous study, CRMP-1, an invasion suppressor gene, was shown to be suppressed in Cl1-5 cells. However, the regulation of CRMP-1 expression has not been explored. In this study, we showed nuclear factor-kappaB controls CRMP-1 expression. The electromobility shift assay showed that while Cl1-0 cells exhibited low NF-kappaB activity in response to TNF-alpha, an abundance of basal and TNF-alpha-induced NF-kappaB-DNA complex was detected in Cl1-5 cells. Supershift-coupled EMSA and Western blotting of nuclear proteins, however, revealed p50 protein, but not classic p65/p50 heterodimer in the complex. ChIP and EMSA demonstrated that p50 binds to a kappaB site residing between -1753 and -1743 of the CRMP-1 promoter region. Transfection of antisense p50 gene into Cl1-5 cells increased the CRMP-1 protein level and decreased the invasive activity of Cl1-5 cells.

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          Author and article information

          Journal
          Biochemical and Biophysical Research Communications
          Biochemical and Biophysical Research Communications
          Elsevier BV
          0006291X
          November 2008
          November 2008
          : 376
          : 2
          : 283-287
          Article
          10.1016/j.bbrc.2008.08.144
          18782567
          30dcd3e2-f1d8-40bd-8f43-cb7e32366e7e
          © 2008

          https://www.elsevier.com/tdm/userlicense/1.0/

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