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Wild-type p53-induced apoptosis in a Burkitt lymphoma cell line is inhibited by interferon gamma

O Sangfelt1, S Einhorn, A C Björklund

  • 1Department of Oncology-Pathology, Karolinska Hospital and Institute, Stockholm, Sweden.

International Journal of Cancer
|July 3, 1996
PubMed

Insights

Gamma interferon (IFN) protects against wild-type p53-induced apoptosis in Burkitt lymphoma cells. This protection was independent of p53, p21, bax, bcl-2, bcl-xL, or c-myc expression levels.

Area of Science:

  • Cellular biology
  • Immunology
  • Cancer research

Background:

  • The tumor suppressor p53 is crucial for regulating cell growth, including apoptosis.
  • Interferons (IFNs) are cytokines known to modulate cellular processes, including apoptosis.

Purpose of the Study:

  • To investigate the effect of gamma-interferon (IFN-γ) and alpha-interferon (IFN-α) on apoptosis induced by wild-type p53.
  • To elucidate the molecular mechanisms underlying IFN-mediated modulation of p53-induced apoptosis.

Main Methods:

  • Utilized a Burkitt lymphoma cell line (BL41) engineered with a temperature-sensitive p53 construct.
  • Assessed the impact of IFN-γ and IFN-α on p53-induced apoptosis and related gene expression.

Main Results:

  • IFN-γ, but not IFN-α, significantly protected cells from wild-type p53-induced apoptosis.
  • This protective effect of IFN-γ was not associated with changes in p53, p21, BAX, BCL-2, BCL-xL, or c-MYC expression.
  • IFN-γ did not alter the expression of the proto-oncogene c-myc.

Conclusions:

  • IFN-γ can suppress apoptosis triggered by wild-type p53.
  • The cellular microenvironment, influenced by cytokines like IFN-γ, plays a critical role in determining the cellular response to p53 activation.

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