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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Published on: April 13, 2015

Downregulation of telomerase reverse transcriptase mRNA expression by wild type p53 in human tumor cells

D Xu1, Q Wang, A Gruber

  • 1Department of Medicine, Division of Hematology, Radiumhemmet, Karolinska Hospital, SE-171 76 Stockholm, Sweden.

Oncogene
|November 7, 2000
PubMed

Insights

The tumor suppressor p53 protein inhibits human telomerase reverse transcriptase (hTERT) expression. This discovery reveals a new mechanism for p53

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Tumor Suppressor Genes

Background:

  • The p53 protein is a critical tumor suppressor involved in cell cycle arrest and apoptosis.
  • Telomerase, particularly its key component human telomerase reverse transcriptase (hTERT), is frequently activated in human cancers, promoting tumorigenesis.

Purpose of the Study:

  • To investigate the role of p53 in regulating human telomerase reverse transcriptase (hTERT) expression.
  • To elucidate the molecular mechanisms by which p53 influences hTERT activity and its implications in tumor suppression.

Main Methods:

  • Activation of exogenous temperature-sensitive p53 and endogenous wild-type p53 in human cancer cell lines (BL41, MCF-7).
  • Analysis of hTERT mRNA expression and the p53 target gene p21.
  • Reporter assays using an hTERT promoter construct in HeLa and Drosophila SL2 cells.
  • Investigation of p53 and Sp1 interaction using co-transfection and binding assays.

Main Results:

  • Activation of p53 led to rapid downregulation of hTERT mRNA expression, independent of p21.
  • Wild-type p53 inhibited hTERT promoter activity in a dose-dependent manner.
  • p53 abrogated Sp1-dependent activation of the hTERT promoter by forming a complex with Sp1, thereby inhibiting Sp1 binding.

Conclusions:

  • Wild-type p53 directly inhibits hTERT expression and telomerase activity.
  • p53-mediated inhibition of hTERT represents a novel mechanism of tumor suppression.
  • These findings enhance understanding of p53's biological functions and hTERT/telomerase regulation in cancer.

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