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NIH 3T3 cells malignantly transformed by mot-2 show inactivation and cytoplasmic sequestration of the p53 protein

R Wadhwa1, S Takano, Y Mitsui

  • 1Chugai Research Institute for Molecular Medicine, Niihari-Mura, Ibaraki, Japan. renu@cimmed.com

Cell Research
|January 11, 2000
PubMed

Insights

High mot-2 protein expression transforms NIH 3T3 cells, inactivating tumor suppressor p53. This mot-2 mediated p53 inactivation contributes to malignant transformation and cellular dysfunction.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Previous studies linked high mot-2 protein expression to NIH 3T3 cell malignant transformation.
  • Mot-2 protein interacts with and inhibits the function of tumor suppressor protein p53.

Purpose of the Study:

  • To investigate the mechanism by which mot-2 contributes to malignant transformation.
  • To determine if mot-2 inactivates p53 function in NIH 3T3 cells.

Main Methods:

  • Stable NIH 3T3 cell lines transfected with mot-2 were analyzed for malignant properties.
  • p53 function was assessed using a p53-dependent reporter assay.
  • p53 expression levels and localization were examined in response to UV irradiation and serum starvation.

Main Results:

  • NIH 3T3 cells expressing mot-2 exhibited malignant characteristics and inactivated p53 function.
  • UV-induced p53 expression was reduced and delayed in NIH 3T3/mot-2 cells.
  • Serum starvation failed to induce nuclear translocation of p53 in NIH 3T3/mot-2 cells.

Conclusions:

  • Mot-2 mediates cytoplasmic sequestration and inactivation of p53.
  • Mot-2-induced p53 inactivation is a contributing factor to the malignant phenotype of NIH 3T3/mot-2 cells.

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