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Updated: Aug 18, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Posttranscriptional changes in growth factor-inducible gene regulation caused by antiproliferative interferons

R A Levine1, T Seshadri, S R Hann

  • 1Department of Biochemistry, Boston University School of Medicine, Massachusetts 02118.

Cell Regulation
|January 1, 1990
PubMed

Insights

Alpha/beta interferon (IFN) inhibits fibroblast proliferation by selectively blocking growth factor-induced gene expression post-transcriptionally. This impacts key proteins, revealing a novel mechanism for interferon

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Growth factors promote cell cycle progression from G0/G1 phase.
  • Interferons (IFNs) inhibit G0/G1 progression through poorly understood mechanisms.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which alpha/beta interferon (IFN) inhibits fibroblast proliferation.
  • To investigate the effect of IFN on growth factor-induced gene expression in murine 3T3 fibroblasts.

Main Methods:

  • Treatment of BALB/c murine 3T3 fibroblasts (A31 cells) with alpha/beta-interferon (IFN).
  • Analysis of messenger ribonucleic acid (mRNA) induction and polysomal accumulation.
  • Measurement of ornithine decarboxylase (odc) enzyme activity and fibronectin protein synthesis.
  • Assessment of c-fos and c-myc protooncogene expression and protein synthesis.

Main Results:

  • IFN did not affect the growth factor-dependent induction of several mRNAs, including odc, fibronectin, c-fos, and c-myc.
  • IFN caused abnormal accumulation of fibronectin and c-myc mRNA on polysomes and increased c-myc mRNA stability.
  • Despite elevated mRNA levels, IFN inhibited serum-stimulated odc enzyme activity and fibronectin protein synthesis.
  • IFN did not affect c-fos protein synthesis but impacted other proteins selectively.

Conclusions:

  • IFN inhibits fibroblast proliferation by suppressing the expression of a subset of growth factor-inducible genes.
  • The inhibitory mechanism involves a selective, posttranscriptional regulation of gene expression by IFN.
  • This study reveals a novel post-transcriptional role for interferons in controlling cell proliferation.

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