Inositol hexakisphosphate kinase 2 mediates growth suppressive and apoptotic effects of interferon-beta in ovarian carcinoma cells

J Biol Chem. 2001 Jul 6;276(27):24965-70. doi: 10.1074/jbc.M101161200. Epub 2001 May 3.

Abstract

Interferons (IFNs) regulate the expression of genes that mediate their antiviral, antitumor, and immunomodulatory actions. We have previously shown that IFN-beta suppresses growth of human ovarian carcinoma xenografts in vivo and induces apoptosis of ovarian carcinoma cells in vitro. To investigate mechanisms of IFN-beta-induced apoptosis we employed an antisense technical knockout approach to identify gene products that mediate cell death and have isolated several regulators of interferon-induced death (RIDs). In this investigation, we have characterized one of the RIDs, RID-2. Sequence analysis revealed that RID-2 was identical to human inositol hexakisphosphate kinase 2 (IP6K2). IP6K2 is post-transcriptionally induced by IFN-beta in ovarian carcinoma cells. A mutant IP6K2 with substitutions in the putative inositol phosphate binding domain abrogates IFN-beta-induced apoptosis. These studies identify a novel function for IP6K2 in cell growth regulation and apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Apoptosis / drug effects*
  • Cell Cycle / drug effects
  • Cell Division / drug effects
  • Consensus Sequence
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Interferon-beta / pharmacology*
  • Isoenzymes / metabolism*
  • Oligonucleotides, Antisense / pharmacology
  • Ovarian Neoplasms / pathology*
  • Phosphotransferases (Phosphate Group Acceptor) / genetics
  • Phosphotransferases (Phosphate Group Acceptor) / metabolism*
  • RNA, Messenger / metabolism
  • Tumor Cells, Cultured

Substances

  • Isoenzymes
  • Oligonucleotides, Antisense
  • RNA, Messenger
  • Interferon-beta
  • Phosphotransferases (Phosphate Group Acceptor)
  • inositol hexakisphosphate kinase