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Related Experiment Videos

Cell transformation by c-Ha-rasVal12 oncogene is accompanied by a decrease in histone H1 zero and an increase in

J Laitinen1, L Sistonen, K Alitalo

  • 1Department of Pathology, University of Helsinki, Finland.

Journal of Cellular Biochemistry
|January 1, 1995
PubMed
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The activated ras oncogene promotes cancer by altering chromatin structure. This transformation leads to decondensation, changes in DNA packaging, and increased vulnerability to mutations, driving cancer development.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • The activated c-Ha-rasVal12 oncogene is implicated in human cancer development.
  • Understanding the molecular mechanisms underlying oncogene-induced transformation is crucial for cancer research.

Purpose of the Study:

  • To investigate the correlation between ras oncogene expression and chromatin structure changes in NIH 3T3 fibroblasts.
  • To explore the impact of ras transformation on nucleosomal repeat lengths and histone H1 zero content.
  • To examine the dynamic changes in chromatin structure upon serum stimulation in normal and ras-transformed cells.

Main Methods:

  • Micrococcal nuclease (MNase) and DNase I digestion assays to assess chromatin decondensation.
  • Analysis of nucleosomal repeat lengths in normal and ras-transformed cells.

Related Experiment Videos

  • Quantification of histone H1 zero content.
  • Serum stimulation and synchronization of cells to study dynamic chromatin changes.

    • Main Results:

    • A positive correlation was observed between the copy number/expression of the c-Ha-rasVal12 oncogene and the degree of chromatin decondensation.
    • Ras transformation altered nucleosomal repeat lengths from 162.3 bp in normal cells to 178.1 bp in transformed cells.
    • Significant changes in histone H1 zero content and rapid, reversible alterations in bulk chromatin structure upon serum stimulation were noted.

    Conclusions:

    • Ras-mediated cell transformation is associated with specific chromatin structural changes, leading to increased vulnerability.
    • These chromatin alterations may predispose cells to further mutations, contributing to cancer development in vivo.
    • Dynamic chromatin remodeling in response to signaling pathways like serum stimulation is linked to transcriptional regulation in both normal and transformed cells.