In:
Molecular Oncology, Wiley, Vol. 3, No. 1 ( 2009-02), p. 54-66
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 β‐catenin, a major player in TCF/lef signaling, is retained in a submembranous location. β‐catenin retention coincided with a subsequent decrease in downstream targets of β‐catenin such as CD44, PLAUR, Myc, cyclin D1 and Met. From these findings we propose a novel model for the suppression of β‐catenin signaling by PCDH24 that leads to contact inhibition.
Type of Medium:
Online Resource
ISSN:
1574-7891
,
1878-0261
DOI:
10.1016/j.molonc.2008.10.005
Language:
English
Publisher:
Wiley
Publication Date:
2009
detail.hit.zdb_id:
2322586-5