Isolation and mutational analysis of a novel human cDNA, DECI (deleted in esophageal cancer I), derived from the tumor suppressor locus in 9q32

Citation
T. Nishiwaki et al., Isolation and mutational analysis of a novel human cDNA, DECI (deleted in esophageal cancer I), derived from the tumor suppressor locus in 9q32, GENE CHROM, 27(2), 2000, pp. 169-176
Citations number
40
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
GENES CHROMOSOMES & CANCER
ISSN journal
10452257 → ACNP
Volume
27
Issue
2
Year of publication
2000
Pages
169 - 176
Database
ISI
SICI code
1045-2257(200002)27:2<169:IAMAOA>2.0.ZU;2-W
Abstract
The long arm of chromosome 9 is thought to contain one or more putative tum or suppressor genes that are mutated in squamous cell carcinomas. This regi on shows frequent loss of heterozygosity (LOH) in carcinomas arising in sev eral developmentally related tissues, including the esophagus, head and nec k, lung, and urinary bladder. We previously delineated the commonly deleted region in a panel of esophageal squamous cell carcinomas to a similar to 2 00 kb genomic segment at 9q32. Here we report the isolation of a novel gene , DEC1 (deleted in esophageal cancer I), from the target region. Mutational analysis of this gene by reverse-transcriptase polymerase chain reaction d isclosed significantly reduced expression of DEC1 in 8 of 13 (62%) esophage al cancer cell lines and in 16 of 30 (53%) primary squamous cell carcinomas of the esophagus. However, no genetic alteration was detected in any of th e cancers examined. Introduction of DEC1 cDNA into 3 cancer cell lines that lacked expression of DEC1 significantly suppressed cell growth, whereas an tisense cDNA or the vector DNA alone did not. Given the reduced expression of the DEC1 gene in esophageal cancer, the high frequency of LOH at 9q32 in esophageal carcinomas, and the fact that the DEC1 cDNA can suppress growth of some cancer cells in vitro, we suggest that the DEC1 gene is a candidat e tumor suppressor in 9q32. Genes Chromosomes Cancer 27: 169-176, 2000. (C) 2000 Wiley-Liss, Inc.