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p56/p53lyn tyrosine kinase activation in mammalian cells treated with mitomycin C

S Kharbanda1, Z M Yuan, N Taneja

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

Oncogene
|October 1, 1994
PubMed

Insights

Mitomycin C (MMC) activates p56/p53lyn tyrosine kinase in leukemia cells, unlike other kinases. This activation is linked to the cell cycle protein p34cdc2, potentially impacting DNA damage response.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Genotoxic agents like mitomycin C (MMC) can induce cellular responses.
  • Protein tyrosine kinases play crucial roles in cell signaling pathways.
  • The activation of specific kinases in response to DNA damage is not fully understood.

Purpose of the Study:

  • To investigate the effects of mitomycin C (MMC) on Src-like protein tyrosine kinases in HL-60 myeloid leukemia cells.
  • To determine the role of p56/p53lyn activation in cellular response to alkylating agents.
  • To elucidate the interaction between activated p56/p53lyn and cell cycle regulatory proteins.

Main Methods:

  • Treatment of HL-60 cells with mitomycin C and other alkylating agents.
  • Assessing the activity of protein tyrosine kinases (p59fyn, pp60c-src, p56/p53lyn) using biochemical assays.
  • Utilizing tyrosine kinase inhibitors (herbimycin A, genistein) to study kinase sensitivity.
  • Employing glutathione S-transferase (GST)-Lyn fusion protein for interaction studies.
  • Performing coimmunoprecipitation and in vitro kinase assays to confirm protein associations and phosphorylation sites.

Main Results:

  • Mitomycin C did not induce p59fyn or pp60c-src activity but rapidly activated p56/p53lyn.
  • Activation of p56/p53lyn involved increased autophosphorylation and sensitivity to kinase inhibitors.
  • p56/p53lyn was found to interact with the cell cycle protein p34cdc2.
  • p34cdc2 showed increased tyrosine phosphorylation upon MMC exposure, with p56/p53lyn phosphorylating Tyr-15 in vitro.

Conclusions:

  • The cellular response to mitomycin C involves the activation of p56/p53lyn.
  • p56/p53lyn activation and its interaction with p34cdc2 may be involved in the DNA damage-dependent mitotic checkpoint signaling.
  • These findings provide insights into the molecular mechanisms of DNA damage response pathways in leukemia cells.

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