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The MDR1 downstream promoter contains sequence-specific binding sites for wild-type p53

B E Strauss1, C Shivakumar, S P Deb

  • 1Department of Pathology, University of California, San Diego, La Jolla 92093-0063, USA.

Insights

Wild-type p53 protein suppresses the human multidrug resistance gene-1 (MDR1) promoter activity. This interaction occurs at the transcriptional level, impacting p-glycoprotein expression.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The p53 protein is a critical tumor suppressor involved in regulating cellular responses to stress.
  • The multidrug resistance gene-1 (MDR1) encodes P-glycoprotein, a transporter protein associated with multidrug resistance in cancer.

Purpose of the Study:

  • To investigate the interaction between wild-type p53 and the promoter region of the human MDR1 gene.
  • To determine if p53 influences MDR1 gene expression.

Main Methods:

  • Reporter gene assays were performed using constructs containing segments of the MDR1 promoter (-189 to +133, -119 to +4, -189 to +4, -2 to +133).
  • Cotransfection assays were conducted in BHK and Saos-2 cell lines with varying amounts of wild-type p53 expression vectors.
  • DNA binding assays were used to demonstrate sequence-specific binding of p53 to the MDR1 promoter.

Main Results:

  • Wild-type p53 demonstrated dose-dependent inhibition of reporter activity driven by the full MDR1 promoter and its isolated segments.
  • Specific DNA segments of the MDR1 promoter were identified as being negatively regulated by wild-type p53.
  • Sequence-specific binding of wild-type p53 protein to the MDR1 promoter was confirmed in vitro.

Conclusions:

  • Wild-type p53 negatively regulates the expression of the MDR1 gene at the transcriptional level.
  • The findings suggest a potential role for p53 in modulating the expression of P-glycoprotein, impacting multidrug resistance.

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