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P53 protein expression in human multidrug-resistant CEM lymphoblasts

N Rafki1, F Liautaud-Roger, L Devy

  • 1GIBSA, Laboratoire de Physiologie Cellulaire, UFR Pharmacie, Université de Reims, France.

Leukemia Research
|February 1, 1997
PubMed

Insights

Multidrug resistance (MDR) involves p53 regulation, but this study found mutant p53 was not overexpressed in resistant cells. Vinblastine treatment increased p53 but not mdm2 or mdr1 expression, suggesting limited p53 regulatory function in MDR.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • The tumor suppressor protein p53 plays a role in regulating multidrug resistance (MDR).
  • Wild-type p53 suppresses the mdr1 promoter, while mutant p53 activates it.
  • Alterations in p53 expression or function are linked to drug resistance.

Purpose of the Study:

  • To investigate p53 and mdm2 protein levels in multidrug-resistant CEM-VLB cells compared to their sensitive CCRF-CEM counterparts.
  • To determine the effect of vinblastine treatment on p53, mdm2, and mdr1 expression in drug-resistant cells.

Main Methods:

  • Western blot analysis to assess p53 and mdm2 protein levels.
  • Quantitative real-time PCR to measure mdr1 mRNA expression.
  • Treatment of cell lines with vinblastine.

Main Results:

  • CEM-VLB cells exhibited increased mdr1 and P-glycoprotein expression but similar p53 and mdm2 protein levels to CCRF-CEM cells.
  • Vinblastine treatment significantly increased p53 protein and mRNA in resistant cells.
  • Vinblastine did not affect mdm2 protein expression or mdr1 mRNA levels in resistant cells.
  • Mutant p53 in these MDR cells did not upregulate mdm2 gene product expression.

Conclusions:

  • Mutant p53 protein was not overexpressed in the studied multidrug-resistant cells.
  • Microtubule-active drug treatment can induce p53 overexpression, but mutant p53 from these MDR cells cannot activate mdm2 expression.
  • The findings suggest a limited role for mutant p53 in regulating mdm2 and mdr1 in this specific MDR model.

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