The elucidation of mechanism of action of PPAR to suppress constitutive NF-kB activity on human myeloma cells

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I indicated that PPARβ could suppress constitutive nuclear factor -κB (NF-κB) activity by PPARβ directly interacted with NF-κB. NF-κB is a dimeric transcription factor that can be formed by the assembly of five diverse proteins, p50, p52, Re1A (p65), Re1B and c-Re1 which, in combination, specify the dimer trancriptional activity. Although there were activated NF-κB in nucleus, in primaly myeloma cells, all NF-κB family was identified in the nucleuses. The PPARβ agonist carbacyclin induced multiple myeloma cell apoptosis. After stimulation of carbacyclin, PPARβ translocated to the nucleus. NF-κB-DNA- binding activity was also decreased in the nucleus of myeloma cell lines. And it was identified PPARβ associated with NF-κB (Re1A/ p65) . These results suggested that PPARβ activation could prevent nucler translocation of NF-κB and decrease the activity of NF-κB binding the promoter of NF-κB target genes in myeloma cell lines.