Adenomatous polyposis coil protein (APC)-independent regulation of beta-catenin/Tcf-4 mediated transcription in intestinal cells

Alterations in the transcriptional activity of the beta-catenin-Tcf complex have been associated with the earlier stages of colonic transformation. We show here that the activation of protein kinase C by the phorbol ester PMA in several intestinal cell lines increases the levels of beta-catenin dete cted in the nucleus and augments the transcriptional activity mediated by b eta-catenin. The response to PMA was not related to modifications in the cy tosolic levels of beta-catenin and was observed not only in cells with wild -type adenomatous polyposis coli protein (APC) but also in APC-deficient ce lls. Binding assays in vitro revealed that PMA facilitates the interaction of the beta-catenin with the nuclear structure. Our results therefore show that beta-catenin-mediated transcription can be regulated independently of the presence of APC.