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See Latest Articlesc-Rel is a transcriptional repressor of EPHB2 in colorectal cancer
The Journal of Pathology, 07/21/09
Fu T et al. - In a trial to investigate the mechanisms that cause EPHB2 down-regulation in colorectal cancer (CRC), it appears that c-Rel acts as a transcriptional repressor of EPHB2 and plays an active role in EPHB2 down-regulation in CRC.
Methods- EPHB2 has recently been identified as a TCF4 transcriptional target that controls the intestinal epithelial architecture through repulsive interactions with Ephrin-B ligands.
- Many reports have demonstrated that most human CRCs lose EPHB2 expression despite constitutive Wnt activation.
- The mechanisms that cause EPHB2 down-regulation in CRC were investigated.
- DNA hypermethylation was not responsible for the frequent loss of EPHB2 expression in CRC.
- Cloning and functional characterization of the EPHB2 gene 5-flanking region revealed a potential negative regulatory element in the distal regulatory region.
- In vitro electrophoretic gel mobility shift and in vivo chromatin immunoprecipitation assays demonstrated that c-Rel directly binds to the putative element.
- Inhibiting c-Rel activity or knocking down c-Rel expression by RNA interference in colon cancer cells was sufficient to induce EPHB2 expression.
- Transient transfection assays demonstrated that c-Rel over-expression repressed endogenous EPHB2 expression in colon cancer cells.
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