Abstract
Our previous findings from a two-hybrid screening essay showed that p68 (DDX5) was a possible partner of CDX2. Research is ongoing to confirm this interaction. We found colocalization of these proteins in nuclei of the colon carcinoma cell line and epithelium of villi. By means of a GST pull-down assay, we revealed that DDX5 was part of the CDX2 complex. During investigation of the effect of DDX5-CDX2 interaction upon β-catenin-mediated transcription, we noted that, in 293T, T98G, and U2OS cells, CDX2 acted as an activator of luciferase expression. In T98G and U2OS cell lines, β-catenin interaction with CDX2 was accompanied by partial decline in transcription-enhancing effect. In these cells, DDX5 acts as a weak repressor, regardless of the interaction with CDX2 and β-catenin. Concerning the influence upon D1 cyclin promoter, we found that, depending on the environment, CDX2 may either suppress (U2OS cells) or enhance its transcription (T98G cells). PDGF reduced both activator and repressor CDX2 activity. In T98G cells cotransfected with DDX5 and CDX2, the repressing activity of DDX5 was inhibited by CDX2 activity. In both cell lines, the native DDX5 acts as a weak repressor of cyclin D1. PDGF treatment does not significantly affect DDX5 activity.
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