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Preferential induction of apoptosis by interferon (IFN)-beta compared with IFN-alpha2: correlation with TRAIL/Apo2L

M Chawla-Sarkar1, D W Leaman, E C Borden

  • 1Center for Drug Discovery and Development, Taussig Cancer Center and Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|June 19, 2001
PubMed

Insights

Interferons (IFNs) induce apoptosis, programmed cell death, in tumor cells. IFN-beta is more effective than IFN-alpha2, partly by upregulating TRAIL, a key protein in initiating apoptosis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oncology

Background:

  • Interferons (IFNs) are known for antiproliferative effects on tumor cells.
  • The precise mechanisms underlying IFN-mediated antitumor activity require further investigation.

Purpose of the Study:

  • To investigate the role of apoptosis in the antitumor effects of Interferon-alpha2 (IFN-alpha2) and Interferon-beta (IFN-beta).
  • To compare the proapoptotic efficacy of IFN-beta and IFN-alpha2 in various cancer cell lines, with a focus on melanomas.

Main Methods:

  • Assessed apoptosis using Annexin V and TUNL staining in response to IFN-alpha2 and IFN-beta.
  • Analyzed caspase cascade activation, cytochrome c release, and DNA fragmentation.
  • Investigated the role of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) induction by IFNs.

Main Results:

  • IFN-beta demonstrated greater growth inhibitory and proapoptotic effects than IFN-alpha2 across tested cell lines.
  • Apoptosis induced by IFN-beta involved caspase cascade activation (caspases 3, 8, 9) and cytochrome c release.
  • IFN-beta induced TRAIL/Apo2L expression in apoptosis-sensitive melanoma cells (WM9), and blocking TRAIL inhibited apoptosis.

Conclusions:

  • IFN-beta effectively induces apoptosis in cancer cells, partly through the activation of the caspase pathway.
  • TRAIL/Apo2L induction by IFN-beta is a significant mechanism contributing to IFN-mediated apoptosis in certain tumor types.
  • These findings reveal a crucial mechanism for the antitumor effects of interferons.

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