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Related Experiment Videos

Lipid signalling pathways in normal and ras-transfected NIH/3T3 cells.

G R Matyas1, P H Fishman

  • 1Laboratory of Molecular and Cellular Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Cellular Signalling
|January 1, 1989
PubMed
Summary

Ras oncogenes do not directly impact phospholipid breakdown in NIH/3T3 cells. Elevated diacylglycerol (DAG) levels in ras-transfected cells are independent of phosphoinositide hydrolysis, suggesting ras alters cell growth via non-lipid signaling pathways.

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Area of Science:

  • Cellular Biology
  • Oncology
  • Molecular Signaling

Background:

  • Ras oncogenes play a critical role in cellular signaling pathways.
  • Phospholipid breakdown is a key event in signal transduction.
  • Understanding ras oncogene involvement in these pathways is crucial for cancer research.

Purpose of the Study:

  • To investigate the role of ras oncogenes in phospholipid breakdown.
  • To determine the relationship between ras oncogenes, diacylglycerol (DAG) levels, and inositol phosphates.
  • To elucidate the signaling mechanisms by which ras oncogenes affect cell growth.

Main Methods:

  • Culturing untransfected and ras-transfected NIH/3T3 cells at varying densities.
  • Measuring diacylglycerol (DAG) and inositol phosphate levels.

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  • Stimulating cells with serum, bombesin, bradykinin, and aluminum fluoride.
  • Treating cells with dibutyryl cyclic AMP (DB-cAMP).

    • Main Results:

    • Ras-transfected cells exhibited elevated DAG levels at low densities, which decreased at high densities.
    • Mutated ras oncogenes, but not proto-H-ras, led to sustained high DAG levels in transformed cells.
    • Basal inositol phosphate levels were unaffected by ras transfection or cell density.
    • Phosphoinositide hydrolysis was differentially stimulated by various agents depending on ras mutation status.
    • DB-cAMP treatment affected DAG levels but not inositol phosphates, and did not alter basal levels.

    Conclusions:

    • The ras gene product p21 is not directly involved in phosphoinositide hydrolysis.
    • Elevated DAG levels in ras-transfected cells are not a consequence of increased phosphoinositide hydrolysis.
    • DAG levels do not correlate with cell growth in normal or ras-transfected NIH/3T3 cells.
    • Ras appears to alter cell growth through mechanisms independent of lipid signaling pathways, specifically phosphoinositide hydrolysis.