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Related Experiment Videos

Morphology of ras-transformed cells becomes apparently normal again with tyrosine kinase inhibitors without a

H J Kwon1, M Yoshida, K Muroya

  • 1Department of Biotechnology, University of Tokyo.

Journal of Biochemistry
|July 1, 1995
PubMed
Summary

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Radicicol, a protein-tyrosine kinase inhibitor, reversed ras-transformed cell morphology by restoring actin stress fibers. This effect requires new gene transcription and protein synthesis, not direct p21ras inhibition.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Ras-transformed cells exhibit altered morphology and actin cytoskeleton organization.
  • Protein-tyrosine kinases play a role in regulating cell growth and transformation.
  • Actin stress fiber restoration is a marker for reversion of the transformed phenotype.

Purpose of the Study:

  • To investigate the effect of radicicol, a protein-tyrosine kinase inhibitor, on ras-transformed cells.
  • To elucidate the mechanism by which radicicol suppresses the transformed phenotype.
  • To determine if radicicol's action involves direct inhibition of p21ras function.

Main Methods:

  • Treatment of v-Ha-ras-transformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells with radicicol.

Related Experiment Videos

  • Assessment of cell morphology and actin stress fiber network.
  • Analysis of p21ras GTP-binding activity and subcellular localization.
  • Inhibition studies using cycloheximide and actinomycin D.

    • Main Results:

    • Radicicol induced morphological reversion in ras-transformed cells, accompanied by restoration of actin stress fibers.
    • No changes were observed in the active GTP-binding form or subcellular localization of p21ras.
    • Co-treatment with cycloheximide or actinomycin D blocked the morphological reversion induced by radicicol.
    • Herbimycin A, another tyrosine kinase inhibitor, produced similar morphological changes.

    Conclusions:

    • Radicicol suppresses the transformed phenotype in ras-transformed cells through a mechanism independent of direct p21ras inhibition.
    • The morphological reversion is dependent on induced gene transcription and de novo protein synthesis.
    • Tyrosine kinase inhibitors represent a potential therapeutic strategy for targeting ras-mutated cancers.