NH2-terminal pentapeptide of endothelial interleukin 8 is responsible for the induction of apoptosis in leukemic cells and has an antitumor effect in vivo

Cancer Res. 1999 Nov 15;59(22):5651-5.

Abstract

We have reported that endothelial interleukin 8 (IL-8) induces apoptosis in leukemic cells in vitro and in vivo, and that interaction between endothelial cells and leukemic cells causes induction of apoptosis through the release of endothelial IL-8 (Y. Terui et al., Biochem. Biophys. Res. Commun., 243: 407-411, 1998; Y. Terui et al., Blood, 92: 2672-2680, 1998). Here, we examined whether a pentapeptide corresponding to the NH2-terminal region of endothelial IL-8 can induce apoptosis in leukemic cells. The NH2-terminal pentapeptide Ala-Val-Leu-Pro-Arg (AVLPR) was found to significantly induce apoptosis in the leukemic cell lines K562, HL-60, Jurkat, and Daudi, as compared with the COOH-terminal pentapeptide Arg-Glu-Ala-Asn-Ser (REANS). Moreover, the NH2-terminal pentapeptide AVLPR significantly inhibited growth of i.p. and s.c. tumor masses of K562 cells and induced apoptosis in these cells in vivo. The active site of endothelial IL-8 is the NH2-terminal pentapeptide AVLPR, and this may serve as a new therapy for hematological malignancies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Cycle
  • Dose-Response Relationship, Drug
  • Drug Screening Assays, Antitumor
  • Humans
  • In Situ Nick-End Labeling
  • Interleukin-8 / chemistry*
  • K562 Cells / drug effects
  • Mice
  • Mice, Nude
  • Oligopeptides / chemistry
  • Oligopeptides / pharmacology*
  • Peptide Fragments / chemistry
  • Peptide Fragments / pharmacology*
  • Tumor Cells, Cultured / drug effects

Substances

  • Interleukin-8
  • Oligopeptides
  • Peptide Fragments
  • alanyl-valyl-leucyl-prolyl-arginine