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LR1 regulates c-myc transcription in B-cell lymphomas

A Brys1, N Maizels

  • 1Department of Molecular Biophysics and Biochemistry, Yale Medical School, New Haven, CT 06510.

Proceedings of the National Academy of Sciences of the United States of America
|May 24, 1994
PubMed

Insights

LR1 protein acts as a transcription factor, activating the c-myc gene in specific B lymphocytes. This discovery suggests LR1 may also influence c-myc translocations in lymphoma.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cancer Biology

Background:

  • LR1 (106-kDa) is a DNA-binding protein initially linked to immunoglobulin class switch recombination in B lymphocytes.
  • The c-myc oncogene is crucial in cell proliferation and is frequently dysregulated in cancers like Burkitt lymphoma.

Purpose of the Study:

  • To investigate the role of LR1 in regulating the human c-myc gene.
  • To determine if LR1 functions as a transcription factor for c-myc.
  • To explore the potential dual role of LR1 in c-myc regulation and translocation.

Main Methods:

  • Site-directed mutagenesis of the LR1 binding site upstream of the c-myc P1 promoter.
  • Reporter gene assays in Burkitt lymphoma cell lines (Raji and BJAB).
  • Bioinformatic analysis to identify LR1 recognition sites in immunoglobulin and c-myc loci.

Main Results:

  • LR1 binds to a DNA site located 310 nucleotides upstream of the human c-myc P1 promoter.
  • Mutation of this LR1 binding site significantly reduced reporter gene expression by 5.5-fold in Raji cells and 3.8-fold in BJAB cells.
  • Multiple LR1 recognition consensus sequences were found at the immunoglobulin heavy-chain locus and the c-myc gene.

Conclusions:

  • LR1 functions as a cell type-specific transcription factor that activates human c-myc expression.
  • The presence of LR1 binding sites in both immunoglobulin and c-myc loci suggests a potential dual role in facilitating c-myc translocations and regulating its transcription.
  • LR1 is implicated in the molecular mechanisms underlying B cell lymphomas.

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