Chronopharmacology of antitumor effect induced by interferon-beta in tumor-bearing mice

J Pharmacol Exp Ther. 2000 Aug;294(2):746-52.

Abstract

The mechanisms underlying the dosing time-dependent change in the antitumor effect of interferon-beta (IFN-beta) were investigated based on the sensitivity of tumor cells and the pharmacokinetics of the drug. Tumor-bearing mice were housed under standardized light-dark cycle conditions (lights on at 7:00 AM, off at 7:00 PM) with food and water available ad libitum. The antitumor effect of IFN-beta (0.5 MI.U./kg, intratumoral) was more efficient in early light phase than in early dark phase. The higher antitumor effect of IFN-beta was observed when specific binding of IFN receptor and DNA synthesis in tumor cells increased, and the lower effect was observed when these levels decreased. The dosing time-dependent effect of IFN-beta was supported by the time-dependent expression of transcription factor (signal transducers and activators of transcription 1) and cell proliferation inhibitor (p21 wild-type p53-activated fragment 1) protein induced by IFN-beta. There was a significant dosing time-dependent change in IFN-beta concentration in tumor, with a higher level in early light phase and a lower level in early dark phase. The dosing time-dependent change of IFN-beta concentration in tumor was associated with that of IFN-beta-induced antitumor effect. These results suggest that by choosing the most suitable dosing time for IFN-beta, the efficacy of the drug can be increased in certain experimental and clinical situations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / administration & dosage*
  • Antineoplastic Agents / pharmacokinetics
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Cell Survival / drug effects
  • Circadian Rhythm / physiology*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / metabolism
  • DNA-Binding Proteins / metabolism
  • Dose-Response Relationship, Drug
  • Drug Administration Schedule
  • Humans
  • Interferon-alpha / metabolism
  • Interferon-beta / administration & dosage*
  • Interferon-beta / pharmacokinetics
  • Male
  • Melanoma, Experimental / drug therapy
  • Melanoma, Experimental / metabolism
  • Melanoma, Experimental / pathology
  • Mice
  • Mice, Inbred C57BL
  • Neoplasm Transplantation
  • Receptor, Interferon alpha-beta
  • Receptors, Interferon / metabolism
  • STAT1 Transcription Factor
  • Trans-Activators / metabolism

Substances

  • Antineoplastic Agents
  • CDKN1A protein, human
  • Cdkn1a protein, mouse
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA-Binding Proteins
  • Interferon-alpha
  • Receptors, Interferon
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • Stat1 protein, mouse
  • Trans-Activators
  • Receptor, Interferon alpha-beta
  • Interferon-beta