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Activation of the c-jun protooncogene in human myeloid leukemia cells treated with etoposide

E Rubin1, S Kharbanda, H Gunji

  • 1Laboratory of Clinical Pharmacology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115.

Molecular Pharmacology
|June 1, 1991
PubMed

Insights

Etoposide, a topoisomerase II inhibitor, transiently induces c-jun protooncogene expression in leukemia cells. This transcriptional induction occurs with DNA damage, suggesting a role in cellular response.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Signaling

Background:

  • Etoposide is a topoisomerase II inhibitor used in cancer therapy.
  • Its effects on gene expression, particularly growth control genes, are not fully understood.

Purpose of the Study:

  • To investigate the impact of etoposide on gene expression, specifically the c-jun protooncogene.
  • To determine the regulatory mechanisms and cellular context of etoposide-induced gene expression.

Main Methods:

  • Utilized HL-60 and U-937 myeloid leukemia cell lines.
  • Employed nuclear run-on assays to assess transcriptional regulation.
  • Monitored gene expression and DNA cleavage patterns.

Main Results:

  • Etoposide induced transient, time-dependent expression of the c-jun protooncogene in both cell lines.
  • Transcriptional regulation was confirmed via nuclear run-on assays.
  • Etoposide-induced c-jun expression correlated with c-fos transcript appearance and DNA cleavage characteristic of programmed cell death.

Conclusions:

  • Transcriptional induction of c-jun is a key cellular response to etoposide-induced DNA damage.
  • This pathway may involve c-fos and is linked to programmed cell death.
  • Etoposide's effects on gene expression provide insights into its mechanism of action in leukemia treatment.

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