Related Experiment Video

Updated: Aug 9, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

Novel interferon-lambdas induce antiproliferative effects in neuroendocrine tumor cells

Kathrin Zitzmann1, Stephan Brand, Sebastian Baehs

  • 1Department of Internal Medicine II, University-Hospital Munich-Grosshadern, University of Munich, Munich, Germany.

Biochemical and Biophysical Research Communications
|May 3, 2006
PubMed

Insights

Novel interferon-lambdas (IL-28A and IL-29) show potent antiproliferative effects on neuroendocrine tumor cells. These interferons activate STAT signaling pathways, suggesting a promising new biotherapy for neuroendocrine carcinomas.

Area of Science:

  • Oncology
  • Immunology
  • Cell Biology

Background:

  • Interferon-alpha (IFN-alpha) is an established biotherapy for neuroendocrine carcinomas.
  • Interferon-lambdas (IFN-lambdas), including IL-28A/B and IL-29, represent a novel class of interferons with potential therapeutic applications.

Purpose of the Study:

  • To investigate the effects of novel interferon-lambdas, specifically IL-28A and IL-29, on human neuroendocrine BON1 tumor cells.
  • To elucidate the signaling pathways and cellular responses induced by IFN-lambdas in this cancer model.

Main Methods:

  • BON1 cells were treated with IL-28A and IL-29 (10 ng/ml).
  • STAT protein phosphorylation (STAT1, STAT2, STAT3) was assessed.
  • Cell proliferation was measured using a proliferation assay.
  • Apoptosis was evaluated by detecting poly(ADP-ribose) polymerase (PARP)-cleavage, caspase-3-cleavage, and DNA fragmentation.
  • The role of suppressor of cytokine signaling proteins (SOCS1 and SOCS3) was investigated through stable overexpression.

Main Results:

  • Incubation with IL-28A and IL-29 induced STAT1, STAT2, and STAT3 phosphorylation in BON1 cells, similar to IFN-alpha.
  • Both IFN-lambdas significantly decreased cell numbers in proliferation assays.
  • Apoptosis was induced, evidenced by PARP-cleavage, caspase-3-cleavage, and DNA fragmentation.
  • Stable overexpression of SOCS1 and SOCS3 abolished these IFN-lambda-induced effects, identifying SOCS proteins as negative regulators.

Conclusions:

  • Novel interferon-lambdas IL-28A and IL-29 exhibit potent antiproliferative effects on neuroendocrine BON1 tumor cells.
  • IFN-lambdas effectively induce STAT signaling and apoptosis in these cells.
  • IFN-lambdas represent a promising new therapeutic strategy for neuroendocrine tumors.

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine09:15

Experimental Melanoma Immunotherapy Model Using Tumor Vaccination with a Hematopoietic Cytokine

Published on: February 24, 2023

Related Concept Videos

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...