Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC

Yoshio Hosoi, Leon N. Kapp, John P. Murnane, Yoshihisa Matsumoto, Atsushi Enomoto, Tetsuya Ono, Kiyoshi Miyagawa

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)728-734
Number of pages7
JournalBiochemical and biophysical research communications
Volume348
Issue number2
DOIs
Publication statusPublished - 2006 Sep 22
Externally publishedYes

Keywords

  • 11q23
  • ATDC
  • Carcinogenesis
  • LOH
  • Suppressor oncogene
  • Transformation

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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