Specific inhibition of c-myc protein biosynthesis using an antisense synthetic deoxy-oligonucleotide in human T lymphocytes

J Immunol. 1988 Apr 1;140(7):2431-5.

Abstract

C-myc protein expression in human T cells was specifically inhibited by a 15-mer deoxy-oligonucleotide complementary to the 5' end of the human c-myc gene second exon. The oligonucleotide penetrates the cells without any treatment, with a plateau of cell association reached in 2 h. The oligonucleotide specifically blocked the de novo synthesis of c-myc protein, induced by PHA in human resting peripheral T cells, without impairing the overall synthesis of other proteins, as shown by two-dimensional analysis of [35S]methionine pulse-labeled proteins. The specific inhibition of c-myc protein synthesis prevented the entry into S phase of resting T cells, induced to proliferate by PHA, or IL-2-dependent T cells induced by IL-2, as shown by [3H]thymidine incorporation. The inhibition of proliferation was specific since it was not observed with the corresponding sense-oligonucleotide and was reversed by preincubation of the cells with an excess of sense oligonucleotide. These results clearly support a role for c-myc protein in the proliferation process and show that inducible protein expression can be blocked by means of synthetic oligonucleotides complementary to a coding exon.

Publication types

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

MeSH terms

  • Gene Expression Regulation / drug effects
  • Humans
  • Interphase / drug effects
  • Lymphocyte Activation / drug effects
  • Oligodeoxyribonucleotides / pharmacology*
  • Protein Synthesis Inhibitors / pharmacology*
  • Proto-Oncogene Proteins / biosynthesis*
  • Proto-Oncogene Proteins c-myc
  • RNA / pharmacology*
  • RNA, Antisense
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*

Substances

  • Oligodeoxyribonucleotides
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-myc
  • RNA, Antisense
  • RNA