p33(ING1) enhances UVB-induced apoptosis in melanoma cells

K-John Cheung1, Gang Li

  • 1Division of Dermatology, Department of Medicine, University of British Columbia, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia, V6H 3Z6, Canada.

Experimental Cell Research
|September 24, 2002
PubMed

Insights

The tumor suppressor ING1 protein (p33ING1) promotes UV-induced apoptosis in melanoma cells. This process requires p53 and involves the mitochondrial pathway, highlighting a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The ING1 tumor suppressor shares functions with p53, including mediating apoptosis.
  • ING1 isoforms, like p33ING1, translocate to the nucleus and interact with PCNA after UV exposure.

Purpose of the Study:

  • To investigate the role of p33ING1 in UV-induced apoptosis in melanoma cells.
  • To elucidate the mechanism by which p33ING1 influences UVB-induced cell death.

Main Methods:

  • Overexpression and antisense plasmid introduction of p33ING1 in melanoma cells.
  • Assessment of apoptosis rates following UVB irradiation.
  • Analysis of p53 dependence, Bax expression, and mitochondrial membrane potential.

Main Results:

  • Overexpression of p33ING1 increased UVB-induced apoptosis, while antisense inhibition reduced it.
  • p33ING1-mediated apoptosis enhancement was dependent on the presence of p53.
  • p33ING1 upregulated Bax expression and altered mitochondrial membrane potential.

Conclusions:

  • p33ING1 acts as a mediator of UVB-induced apoptosis in melanoma.
  • p33ING1 cooperates with p53 through the mitochondrial cell death pathway in response to UVB.
  • These findings suggest p33ING1 as a potential target for melanoma treatment.

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