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A ras-related gene with transformation suppressor activity

H Kitayama1, Y Sugimoto, T Matsuzaki

  • 1Laboratory of Molecular Oncology, Tsukuba Life Science Center, Ibaraki, Japan.

Cell
|January 13, 1989
PubMed

Insights

Researchers identified the Krev-1 gene, which suppresses cancer cell growth and shares similarities with ras proteins. This gene is found across species and widely expressed, suggesting a crucial role in tissue regulation.

Area of Science:

  • Molecular biology
  • Cell biology
  • Genetics

Background:

  • Kirsten sarcoma virus transformation of NIH/3T3 cells leads to a malignant phenotype.
  • Identifying genes that can reverse this transformation is crucial for understanding cancer biology.

Purpose of the Study:

  • To isolate and characterize a cDNA clone with the ability to reverse the transformed phenotype of NIH/3T3 cells.
  • To investigate the function and evolutionary conservation of the identified gene.

Main Methods:

  • Isolation of a cDNA expression library from human fibroblasts.
  • Transfection of NIH/3T3 cells with the Krev-1 cDNA clone.
  • Analysis of mRNA levels and phenotypic suppression.
  • Amino acid sequence comparison with known proteins.
  • Southern blot analysis to detect homologous sequences in other species.

Main Results:

  • A 1.8 kb cDNA clone, Krev-1, was isolated and demonstrated revertant-inducing activity.
  • Krev-1 transfectants showed a correlation between specific mRNA levels and suppression of the transformed phenotype.
  • The Krev-1 cDNA encodes a 21,000-dalton protein with approximately 50% amino acid identity to ras proteins.
  • Homologous Krev-1 sequences were detected in mouse, rat, and chicken DNA, with ubiquitous expression in rat organs.

Conclusions:

  • The Krev-1 gene plays a significant role in various tissues.
  • Krev-1 may be involved in the negative regulation of cell growth in specific cell types.
  • The structural similarity to ras proteins suggests a potential role in cellular signaling pathways related to growth control.

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