Browse by author
Lookup NU author(s): Dr Gordon Strathdee
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
We identified CAVEOLIN-1 as a candidate for a tumour suppressor gene mapping to human chromosome 7q31.1. A number of studies suggest that caveolin could function as a tumour suppressor. Expression of caveolin, and in turn the number of caveolae within a cell, are inversely correlated with the transforming ability of numerous oncoproteins, including H-ras, v-abl, and bcr-abl, and caveolin is a major transformation-dependent substrate of v-src. Heterologous expression of caveolin has been shown to abrogate anchorage-independent growth and induce apoptosis in transformed fibroblasts and also to suppress anchorage-independent growth in human mammary carcinoma cells. We have analysed the status and expression of the human CAVEOLIN-1 gene in primary tumours and tumour-derived cell lines. We found no evidence for mutation of CAVEOLIN-1 in human cancers. Additionally, we found that while the first two exons of CAVEOLIN-1 are associated with a CpG island, this is not methylated in either primary tumours or in tumour-derived cell lines in which Caveolin-1 expression is low or undetectable. The level of expression of Caveolin-1 does not correlate with loss of heterozygosity at the CAVEOLIN-1 locus in these same cell lines. Contrary to other published studies, we have shown that CAVEOLIN-1 is not expressed in normal breast ductal epithelial cells in vivo. CAVEOLIN-1 is however highly expressed in breast myoepithelial cells and its expression is retained in tumours derived from breast myoepithelium. Together our data refute a role for CAVEOLIN-1 as a breast tumour suppressor gene in vivo.
Author(s): Strathdee G; Hurlstone AF; Reid G; Reeves JR; Fraser J; Rahilly M; Parkinson EK; Black DM
Publication type: Article
Publication status: Published
Journal: Oncogene
Year: 1999
Volume: 18
Issue: 10
Pages: 1881-1890
Print publication date: 01/03/2011
ISSN (print): 0950-9232
ISSN (electronic): 1476-5594
Publisher: Stockton Press
URL: http://dx.doi.org/10.1038/sj.onc.1202491
DOI: 10.1038/sj.onc.1202491
Notes: Journal Article Research Support, Non-U.S. Gov't England
Altmetrics provided by Altmetric