Anti-ICAT polyclonal antibody

Deregulation of the pRb/E2F or Wnt/beta-catenin pathway occurs frequently in human cancers, which is often associated with inappropriate cell proliferation. Although the oncogenic roles of pRb/E2F1 and Wnt/beta-catenin pathways have been well studied, the functional interaction between the two pathways has only recently been characterized. In particular, E2F1 has been recently reported to negatively regulate Wnt/beta-catenin activity in human colorectal cancers, though the mechanism underlying this regulation is not fully understood. Here we provide evidence that beta-catenin interacting protein 1 (CTNNBIP1), also known as ICAT (inhibitor of beta-catenin and TCF4), functions as a crucial node to mediate the cross talk between E2F1 and beta-catenin signaling. We show that ICAT is a direct transcriptional target of E2F1, and that activation of ICAT by E2F1 is required for E2F1 to inhibit beta-catenin activity. This study provides a mechanistic insight into the antagonistic interaction between E2F1 and beta-catenin signaling. Oncogene (2011) 30, 3979-3984; doi:10.1038/onc.2011.129; published online 2 May 2011

Soybean isoflavonoids have received significant attention due to their potential anticarcinogenic and antiproliferative effects and possible role in many signal transduction pathways. However, their mechanisms of action and their molecular targets remain to be further elucidated. In this paper, we demonstrated that two soybean isoflavones (genistein and daidzein) reduced the proliferation of the human colon adenocarcinoma grade II cell line (HT-29) at concentrations of 25 and 50-100 mu M, respectively. We then investigated the effects of genistein and daidzein by RT-PCR on molecules that involved in tumor development and progression by their regulation of cell proliferation. At a concentration of 50 mu M genistein, there was suppressed expression of beta-catenin (CTNNBIP1). Neither genistein nor daidzein affected APC (adenomatous polyposis coli) or survivin (BIRC5) expression when cells were treated with concentrations of 10 or 50 mu M. These data suggest that the down-regulation of beta-catenin by genistein may constitute an important determinant of the suppression of HT-29 cell growth and may be exploited for the prevention and treatment of colon cancer.