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Transcriptional activation of bovine mimecan by p53 through an intronic DNA-binding site

E S Tasheva1, C G Maki, A H Conrad

  • 1Division of Biology, Kansas State University, Manhattan 66506-4901, USA. est@ksu.edu

Biochimica Et Biophysica Acta
|May 9, 2001
PubMed

Insights

This study reveals that the mimecan gene is regulated by the p53 protein. Mimecan expression is reduced in tumors, suggesting a role for mimecan in cancer, linked to the p53 network.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cancer Biology

Background:

  • Mimecan, a small leucine-rich proteoglycan, exists as a keratan sulfate proteoglycan or glycoprotein.
  • Transcriptional regulation of mimecan was previously unknown.
  • Eight mimecan mRNA transcripts, encoding a single protein, are generated through alternative RNA processing.

Purpose of the Study:

  • To investigate the transcriptional regulation of the mimecan gene.
  • To determine the relationship between mimecan and the p53 tumor suppressor network.

Main Methods:

  • Identified a conserved p53-binding DNA sequence in the first intron of human and bovine mimecan genes.
  • Performed in vitro binding assays with wild-type p53 and mimecan DNA sequence.
  • Utilized co-transfection assays with mimecan promoter-luciferase constructs and p53 expression vectors in various cell lines.

Main Results:

  • Wild-type p53 demonstrated binding to the identified consensus sequence in vitro.
  • Co-transfection experiments showed activation of the mimecan promoter via the p53-binding sequence.
  • Mimecan expression was found to be absent in multiple tumor types and cancer cell lines with inactivated p53.

Conclusions:

  • This study establishes a novel link between mimecan and the p53 regulatory network.
  • The findings suggest that mimecan may function as a tumor suppressor gene regulated by p53.
  • Further research into mimecan's role in cancer biology is warranted.

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