Abstract
MED28, a Mediator subunit for transcriptional activation, interacts with multiple proteins, including merlin, actin cytoskeleton, and Grb2. MED28 is often highly expressed in colorectal, breast, and prostate cancers. HMG box‐containing protein 1 (HBP1), a transcriptional repressor, inhibits Wnt/β‐catenin signaling by blocking the binding of β‐catenin to the TCF/LEF transcription factors and reducing the expression of cyclin D1 and c‐Myc. Previously our laboratory found that MED28 modulates cell growth through HBP1 in breast cancer; the objective of the current study is to investigate the putative role of MED28/HBP1 in colorectal cancer. Suppression of MED28 increased the expression of HBP1, but reduced the expression of cyclin D1 and c‐Myc in HCT116 and SW480 colon cancer cells. The reporter activity of an HBP1 promoter increased upon MED28 knockdown. Moreover, suppression of MED28 resulted in β‐catenin translocation from nucleus to cytoplasm, corresponding to a lower transcriptional activity of the TOPflash reporter construct. Out data indicate that MED28 hinders the repressive effect of HBP1, and, thereby, activates the Wnt/β‐catenin pathway in colorectal cancer.Grant Funding Source: Supported by NSC101‐2320‐B‐309‐001 and NSC102‐2320‐B‐309‐001‐MY3 to M‐F Lee
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