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Inhibition of tumor cell growth by RTP/rit42 and its responsiveness to p53 and DNA damage

S K Kurdistani1, P Arizti, C L Reimer

  • 1Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA.

Cancer Research
|October 10, 1998
PubMed

Insights

Reduced in tumor 42 (rit42), also known as homocysteine-inducible gene (RTP), is a growth inhibitory gene. Its diminished expression in cancer cells suggests a role in tumor development.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • A novel cDNA clone, rit42 (reduced in tumor, 42 kDa), was identified via differential screening.
  • This gene is also known as RTP (homocysteine-inducible gene in human endothelial cells) and is androgen-responsive in mice.

Purpose of the Study:

  • To investigate the role of rit42/RTP in normal versus tumor cells.
  • To understand the cell cycle regulation and p53 dependency of rit42/RTP expression.
  • To evaluate the therapeutic potential of rit42/RTP in cancer.

Main Methods:

  • Differential screening, Northern blot analysis, in situ hybridization.
  • Cell culture, in vitro and in vivo tumor growth assays.
  • p53-inducible system analysis, immunofluorescence, chromosome localization.

Main Results:

  • rit42/RTP expression is significantly diminished in various tumor cells (breast, prostate) compared to normal cells.
  • rit42/RTP mRNA expression cycles with cell division in normal cells but this is absent in tumor cells.
  • Introduction of rit42 cDNA inhibited cancer cell growth in vitro and in vivo.
  • rit42/RTP expression is induced by DNA-damaging agents in a p53-dependent manner.
  • The protein localizes to the cytoplasm and translocates to the nucleus upon DNA damage.

Conclusions:

  • rit42/RTP exhibits growth inhibitory functions.
  • Down-regulation of rit42/RTP may contribute to tumor progression.
  • rit42/RTP represents a potential therapeutic target for cancer treatment.

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