The GRIMs: a new interface between cell death regulation and interferon/retinoid induced growth suppression

Cytokine Growth Factor Rev. 2004 Apr-Jun;15(2-3):169-94. doi: 10.1016/j.cytogfr.2004.01.002.

Abstract

Cytokines and vitamins play a central role in controlling neoplastic cell growth. The interferon (IFN) family of cytokines regulates antiviral, anti-tumor, antimicrobial, differentiation, and immune responses in mammals. Significant advances have been made with respect to IFN-induced signal transduction pathways and antiviral responses. However, the IFN-induced anti-tumor actions are poorly defined. Although IFNs themselves inhibit tumor growth, combination of IFNs with retinoids (a class of Vitamin A related compounds) strongly potentiates the IFN-regulated anti-tumor action in a number of cell types. To define the molecular mechanisms involved in IFN/retinoid (RA)-induced apoptosis we have employed a genetic approach and identified several critical genes. In this review, I provide the current picture of IFN- RA- and IFN/RA-regulated growth suppressive pathways. In particular, I focus on a novel set of genes, the genes-associated with retinoid-interferon induced mortality (GRIM). GRIMs may be novel types of tumor suppressors, useful as biological response markers and potentially novel targets for drug development.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins
  • Apoptosis*
  • Cell Division
  • Humans
  • Interferons / genetics
  • Interferons / physiology*
  • NADH, NADPH Oxidoreductases / physiology*
  • Retinoids / genetics
  • Retinoids / physiology*
  • Signal Transduction
  • Transcription Factors / metabolism
  • Tretinoin / metabolism

Substances

  • Apoptosis Regulatory Proteins
  • Retinoids
  • Transcription Factors
  • Tretinoin
  • Interferons
  • NADH, NADPH Oxidoreductases
  • NDUFA13 protein, human