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Related Experiment Videos

A colchicine-sensitive uptake system in Morris hepatomas.

R Tauber, W Reutter

    Proceedings of the National Academy of Sciences of the United States of America
    |September 1, 1980
    PubMed
    Summary

    Microtubule disruptors like colchicine significantly inhibit amino acid uptake in hepatomas, but not in normal liver cells. This suggests a unique, microtubule-dependent transport system in cancerous liver cells.

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    Area of Science:

    • Biochemistry
    • Cell Biology
    • Oncology

    Background:

    • Amino acid and substrate uptake are crucial for cellular function.
    • Microtubules play roles in various cellular processes, including transport.
    • Hepatomas exhibit altered metabolic pathways compared to normal liver tissue.

    Purpose of the Study:

    • To investigate the effect of microtubular disruptors on substrate uptake in hepatomas.
    • To determine if hepatoma cell transport mechanisms differ from host and regenerating liver.
    • To explore the role of microtubules in hepatoma substrate transport.

    Main Methods:

    • Treatment of Morris hepatomas, host liver, and regenerating liver with microtubular disruptors (colchicine, vinblastine, lumicolchicine, cytochalasin B).
    • Measurement of amino acid (alpha-aminoisobutyric acid, L-methionine, L-leucine) and substrate uptake.
    • Assessment of cellular ATP and UTP levels.

    Main Results:

    • Colchicine inhibited amino acid transport in hepatomas by 59-98%.
    • Host and regenerating liver showed increased, not inhibited, amino acid transport with colchicine.
    • Vinblastine was an effective inhibitor; lumicolchicine and cytochalasin B were not.
    • Inhibition was independent of cellular ATP and UTP levels.

    Conclusions:

    • Hepatoma substrate transport is sensitive to colchicine, suggesting a link to microtubules or other colchicine-binding structures.
    • A distinct, microtubule-dependent uptake system may exist in hepatoma cells.
    • This altered transport system could be a consequence of malignant transformation in hepatocytes.

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