PCDH24-induced contact inhibition involves downregulation of beta-catenin signaling.

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,

SUBMITTER: Ose R 

PROVIDER: S-EPMC5527873 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature