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Updated: Jun 23, 2026

Reconstitution Of β-catenin Degradation In Xenopus Egg Extract
Published on: June 17, 2014
PCDH24-induced contact inhibition involves downregulation of beta-catenin signaling
Rui Ose1, Toshihide Yanagawa, Shun Ikeda
1Laboratory of Medical Genomics, Department of Human Genome Research, Kazusa DNA Research Institute, 2-6-7 Kazusa-Kamatari, Kisarazu, Chiba 292-0818, Japan.
Abstract:
Elevated expression of the protocadherin LKC (PCDH24) in HCT116 colon carcinoma cells has been shown to induce contact inhibition, thereby completely abolishing tumor formation in vivo (Carcinogenesis, 2002; 23(7):1139-1148). To clarify the molecular mechanism behind this effect, we performed 2-DE/MS and DNA microarray analyses in order to compare protein and gene expression patterns of parental HCT116 and PCDH24-expressing HTC116 derivative cells. The data revealed drastic changes in phenotypic markers between parental and PCDH24-expressing cells. We found that in PCDH24-expressing cells beta-catenin, a major player in TCF/lef signaling, is retained in a submembranous location. beta-catenin retention coincided with a subsequent decrease in downstream targets of beta-catenin such as CD44, PLAUR, Myc, cyclin D1 and Met. From these findings we propose a novel model for the suppression of beta-catenin signaling by PCDH24 that leads to contact inhibition.
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