A novel strategy of c-myc oncogene in NK activity regulation not related to the W6/32 MHC class-I epitope

Int J Cancer. 1994 Jul 1;58(1):123-8. doi: 10.1002/ijc.2910580120.

Abstract

The c-myc gene encodes a nuclear protein whose precise function is still not fully understood. Introduction of a c-myc gene into a number of cell lines leads to an increase in their susceptibility to NK-cell lysis. It was reported earlier that c-myc can induce a decrease in the membrane expression of the MHC class-I molecules and this may be one of the factors that render target cells relatively more susceptible to NK lysis. In this contribution, we show, in a human LCL line transfected with a constitutively active c-myc gene, an increased sensitivity to NK lysis, which correlates with an augmented effector-target binding ability of c-myc-transfected LCLs and with a high ICAM-I expression rather than with down-regulation of MHC class-I W6/32 epitope expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Surface / genetics
  • Antigens, Surface / physiology
  • Blotting, Northern
  • Callithrix
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / physiology
  • Cell Transformation, Viral
  • Cold Temperature
  • Cytotoxicity, Immunologic
  • Epitopes / physiology*
  • Gene Expression
  • Genes, myc / physiology*
  • Herpesvirus 4, Human
  • Histocompatibility Antigens Class I / immunology
  • Histocompatibility Antigens Class I / physiology*
  • Humans
  • Intercellular Adhesion Molecule-1
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / physiology*
  • Lymphoma / genetics
  • Lymphoma / immunology
  • Methods
  • Mice
  • Phenotype
  • Transfection

Substances

  • Antigens, Surface
  • Cell Adhesion Molecules
  • Epitopes
  • Histocompatibility Antigens Class I
  • Intercellular Adhesion Molecule-1