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

Yoshio Hosoi1, Leon N Kapp, John P Murnane

  • 1Department of Radiation Research, Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan. hosoi@m.u-tokyo.ac.jp

Biochemical and Biophysical Research Communications
|August 8, 2006
PubMed

Insights

The ataxia-telangiectasia group D complementing gene (ATDC) plays a role in preventing cancer. Suppressed ATDC expression correlates with a malignant phenotype, suggesting its tumor-suppressive function.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The ataxia-telangiectasia group D complementing gene (ATDC) is located at 11q23, a region frequently affected by loss of heterozygosity (LOH) in various cancers, including breast cancer.
  • Previous studies indicate ATDC underexpression in breast and prostate cancers and that SV-40 transformation down-regulates ATDC expression.

Purpose of the Study:

  • To investigate the role of ATDC in the process of carcinogenesis.
  • To examine ATDC expression levels in various cancer cell lines.

Main Methods:

  • Assessed ATDC expression (mRNA and protein) in 11 cancer cell lines.
  • Transfected ATDC expression vectors into Saos-2 and BT-549 cell lines lacking detectable ATDC.
  • Evaluated the effect of ATDC re-expression on colony-forming efficiency in soft agar.

Main Results:

  • No detectable ATDC transcript was observed in 4 tumor cell lines.
  • No ATDC protein was detected in 8 tumor cell lines.
  • Transfection of ATDC significantly suppressed colony-forming efficiency in soft agar in the recipient cell lines.

Conclusions:

  • Suppressed expression of ATDC is associated with a malignant cellular phenotype.
  • These findings suggest that ATDC functions as a tumor suppressor gene.

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