Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC.
The ataxia-telangiectasia group D complementing gene, ATDC, is located at 11q23, where loss of heterozygosity (LOH) is frequently observed in many kinds of cancers including breast cancer. Underexpression of ATDC in breast and prostate cancer has been reported using serial analysis of gene expression (SAGE) and DNA microarray analysis. We previously reported that SV-40-transformation down-regulates the expression of ATDC. In the present study, we investigated the roles of ATDC in carcinogenesis. First, we investigated the expression of ATDC in 11 cancer cell lines. No detectable transcript was observed in 4 tumor cell lines, and no ATDC protein was detected in 8 tumor cell lines. We transfected ATDC expression vector into Saos-2 and BT-549 that lacked detectable mRNA and protein expression of ATDC. Colony-forming efficiency in soft agar was significantly suppressed in all of the ATDC transfectants. These results suggest that suppressed ATDC expression is associated with malignant phenotype.
Hosoi
Yoshio
Y
Department of Radiation Research, Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan. hosoi@m.u-tokyo.ac.jp
Kapp
Leon N
LN
Murnane
John P
JP
Matsumoto
Yoshihisa
Y
Enomoto
Atsushi
A
Ono
Tetsuya
T
Miyagawa
Kiyoshi
K
D045744:Cell Line, Tumor / Q000166:cytology; D049109:Cell Proliferation; D002472:Cell Transformation, Viral; D004268:DNA-Binding Proteins / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D013539:Simian virus 40; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics; D014162:Transfection; D014410:Tumor Stem Cell Assay
D004268:DNA-Binding Proteins; C087296:TRIM29 protein, human; D014157:Transcription Factors