1999/01/05 by Yinhua Yu, Fengji Xu, Hongqi Peng +9 · 292 citations
Biochemistry, Genetics and Molecular Biology · Medicine · #Allele #Biology #Breast cancer #Cancer #Cancer research #Carcinogenesis #Cell #Cell cycle #Clonogenic assay #Cyclin D1 #DNA methylation #Epigenetics and DNA Methylation #Gene #Gene expression #Gene silencing #Genetic Syndromes and Imprinting #Genetics #Genomic imprinting #Loss of heterozygosity #Ovarian cancer #Prenatal Screening and Diagnostics #Tumor suppressor gene
paper · doi:10.1073/pnas.96.1.214
published in Proceedings of the National Academy of Sciences 96(1), 214-219 (National Academy of Sciences)
openalex publication_date 1999/01/05 · openalex created_date 2016/06/24 · openalex updated_date 2026/08/01
Using differential display PCR, we have identified a gene [NOEY2, ARHI (designation by the Human Gene Nomenclature Committee)] with high homology to ras and rap that is expressed consistently in normal ovarian and breast epithelial cells but not in ovarian and breast cancers. Reexpression of NOEY2 through transfection suppresses clonogenic growth of breast and ovarian cancer cells. Growth suppression was associated with down-regulation of the cyclin D1 promoter activity and induction of p21(WAF1/CIP1). In an effort to identify mechanisms leading to NOEY2 silencing in cancer, we found that the gene is expressed monoallelically and is imprinted maternally. Loss of heterozygosity of the gene was detected in 41% of ovarian and breast cancers. In most of cancer samples with loss of heterozygosity, the nonimprinted functional allele was deleted. Thus, NOEY2 appears to be a putative imprinted tumor suppressor gene whose function is abrogated in ovarian and breast cancers.