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Decrease in 5'-nucleotidase activity in malignant transformed and normal stimulated cells.

A Raz, J G Collard, M Inbar

    Cancer Research
    |May 1, 1978
    PubMed
    Summary
    This summary is machine-generated.

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    Malignant cells and stimulated normal cells show significantly reduced 5'-nucleotidase activity compared to normal cells. This specific enzyme alteration in surface membranes is not observed with acid phosphatase.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Oncology

    Background:

    • 5 -nucleotidase is an enzyme crucial for cell membrane function.
    • Alterations in enzyme activity are often associated with cellular transformation and disease.

    Purpose of the Study:

    • To investigate the specific activity of 5 -nucleotidase in normal, transformed, and stimulated cells.
    • To determine if changes in 5 -nucleotidase activity are specific to malignant transformation or cellular stimulation.

    Main Methods:

    • Enzyme assays were performed on various cell types, including fibroblasts and lymphocytes.
    • Cells were analyzed in both normal and pathological (malignant, leukemic) states.
    • Stimulation protocols using serum and concanavalin A were employed for normal cells.

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    Main Results:

    • A significant decrease (3- to 30-fold) in 5 -nucleotidase specific activity was observed in malignant cells compared to normal counterparts.
    • Serum stimulation of fibroblasts and concanavalin A stimulation of lymphocytes led to decreased 5 -nucleotidase activity.
    • Acid phosphatase activity remained unchanged in stimulated and malignant cells, indicating specific 5 -nucleotidase alteration.

    Conclusions:

    • 5 -nucleotidase activity is specifically reduced in malignant cells and in normal cells upon stimulation.
    • The observed decrease in 5 -nucleotidase is a specific membrane alteration, not a general enzymatic change.
    • This finding suggests a potential role for 5 -nucleotidase in cellular transformation and response to stimuli.