Interferon-alpha inhibits proliferation and induces apoptosis of merkel cell carcinoma in vitro

Cancer Invest. 2008 Jul;26(6):562-8. doi: 10.1080/07357900701816477.

Abstract

Merkel cell carcinoma is a tumor with aggressive biological behavior and limited response to chemotherapy. The present study investigated the effect of interferon (IFN)-alpha on growth and apoptosis of Merkel carcinoma cells in vitro. Proliferation of MCC-1 cell line was reduced dose-dependently by IFN-alpha and diminished when higher IFN-alpha concentrations were used. Additionally, IFN-alpha potently decreased DNA-synthesis and Ki67/MIB-1 proliferation index of MCC-1 cultures. Furthermore, IFN-alpha induced dose-dependently apoptosis of MCC-1 cells as shown by caspase-3 activation, and detection of apoptotic DNA strand breaks and fragmented nuclei. These findings suggest that IFN-alpha may have antitumor activity against Merkel cell carcinoma.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Carcinoma, Merkel Cell / metabolism
  • Carcinoma, Merkel Cell / pathology*
  • Caspase 3 / metabolism
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • DNA Breaks
  • DNA Replication / drug effects
  • Dose-Response Relationship, Drug
  • Enzyme Activation
  • Humans
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Interferon alpha-2
  • Interferon-alpha / metabolism
  • Interferon-alpha / pharmacology*
  • Ki-67 Antigen / metabolism
  • Merkel Cells / drug effects*
  • Merkel Cells / metabolism
  • Merkel Cells / pathology
  • Receptor, Interferon alpha-beta / drug effects
  • Receptor, Interferon alpha-beta / metabolism
  • Recombinant Proteins
  • Skin Neoplasms / metabolism
  • Skin Neoplasms / pathology*
  • Time Factors

Substances

  • Antineoplastic Agents
  • Interferon alpha-2
  • Interferon-alpha
  • Ki-67 Antigen
  • Recombinant Proteins
  • Receptor, Interferon alpha-beta
  • CASP3 protein, human
  • Caspase 3