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Related Experiment Videos

Dolichol biosynthesis in human malignant cells.

A Henry1, P W Stacpoole, C M Allen

  • 1Department of Biochemistry and Molecular Biology, College of Medicine, J. Hillis Miller Health Center, University of Florida, Gainesville 32610.

The Biochemical Journal
|September 15, 1991
PubMed
Summary
This summary is machine-generated.

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Malignant cells show increased mevalonate pathway activity but produce shorter-chain dolichols compared to normal cells. This difference in dolichol chain length is specific to certain cancers, including leukemia and hepatoma.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Cancer Research

Background:

  • Mevalonic acid is a precursor for cholesterol, ubiquinone, and dolichol biosynthesis.
  • Aberrant lipid metabolism is a hallmark of cancer cells.
  • Dolichols are involved in protein glycosylation, a process often altered in cancer.

Purpose of the Study:

  • To investigate the biosynthesis of cholesterol, ubiquinone, and dolichol from mevalonic acid in various human cancer cells.
  • To compare the relative flux and product distribution of mevalonate metabolism between malignant and non-malignant cells.
  • To analyze the chain length of synthesized dolichols in different cellular contexts.

Main Methods:

  • Culturing of non-malignant and malignant human lymphocytes and human hepatoma cells.

Related Experiment Videos

  • Isolation of human mononuclear leucocytes from peripheral blood.
  • Measurement of mevalonic acid incorporation into cholesterol, ubiquinone, and dolichol.
  • Analysis of dolichol chain length using chromatographic methods.

    • Main Results:

    • Malignant cultured cells exhibited an order of magnitude greater incorporation of mevalonate into lipids compared to non-malignant cells.
    • The relative distribution of mevalonate into cholesterol, ubiquinone, and dolichol was similar between malignant and non-malignant cells.
    • Leukaemic cells, hepatoma cells, and mononuclear leucocytes from leukaemia patients predominantly synthesized shorter-chain dolichols.

    Conclusions:

    • Cancer cells display enhanced mevalonate pathway activity but not altered product partitioning.
    • A specific defect in dolichol chain elongation occurs in certain malignancies, including leukemia and hepatoma.
    • Normal dolichol chain length is maintained in non-tumorigenic cells and cells from non-hematological malignancies.