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Elevated c-myc expression in progeria fibroblasts.

K D Nakamura1, A Turturro, R W Hart

  • 1Food and Drug Administration, National Center for Toxicological Research, Jefferson, AR 72079.

Biochemical and Biophysical Research Communications
|September 15, 1988
PubMed
Summary
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Hutchinson-Gilford Syndrome (Progeria) cells show elevated c-myc protooncogene expression. This finding in progeria fibroblasts suggests a potential role for c-myc in this premature aging disorder.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Hutchinson-Gilford Syndrome (Progeria) is a rare genetic disorder characterized by premature aging.
  • Protooncogenes play critical roles in cell growth and differentiation.
  • Altered protooncogene expression is implicated in various diseases, including cancer and aging.

Purpose of the Study:

  • To investigate protooncogene expression in cultured human fibroblasts from Progeria patients.
  • To determine if specific protooncogenes, such as c-myc, c-erbB, and c-src, are differentially expressed in Progeria cells compared to normal controls.

Main Methods:

  • Cultured human fibroblasts from Progeria donors and age-matched controls were utilized.
  • Quantitative analysis of protooncogene expression levels was performed.

Related Experiment Videos

  • Southern blot analysis was used to assess gene amplification or translocation.

    • Main Results:

    • Significantly increased c-myc protooncogene expression was observed in Progeria fibroblasts (up to 150% increase).
    • A non-classic Progeria case showed a moderate increase (45%) in c-myc expression.
    • Southern blot analysis ruled out c-myc gene amplification or translocation as the cause of increased expression.
    • No significant differences in c-erbB or c-src protooncogene expression were detected between Progeria and control cells.

    Conclusions:

    • Elevated c-myc expression is a characteristic feature of classic Progeria fibroblasts.
    • The increased c-myc expression in Progeria is not due to gene amplification or translocation.
    • These findings suggest a potential involvement of the c-myc protooncogene in the pathogenesis of Hutchinson-Gilford Syndrome.