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Updated: May 30, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Wild-type p53 controls cell motility and invasion by dual regulation of MET expression

Chang-Il Hwang1, Andres Matoso, David C Corney

  • 1Department of Biomedical Sciences, Microarray Core Facility, Cornell University, Ithaca, NY 14853, USA.

Proceedings of the National Academy of Sciences of the United States of America
|August 12, 2011
PubMed

Insights

Mutant p53 promotes cancer spread by increasing MET receptor tyrosine kinase. Inhibiting MET may treat p53-mutated cancers, revealing a key p53/MET regulatory network in tumor invasion.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • p53 mutations are linked to tumor growth and metastasis.
  • Mechanisms of p53's role in cell motility and invasion are not fully understood.

Purpose of the Study:

  • To investigate the role of p53 in regulating cell motility and invasion.
  • To identify molecular mechanisms linking p53 status to invasive properties.

Main Methods:

  • Utilized primary ovarian surface epithelium cell cultures.
  • Examined the effects of p53 inactivation or mutation on MET receptor tyrosine kinase expression.
  • Assessed MET-dependent cell motility and invasion.
  • Investigated p53's regulation of MET via miR-34 and SP1 binding to the MET promoter.

Main Results:

  • Conditional p53 inactivation or expression of mutant p53 led to MET receptor tyrosine kinase overexpression.
  • Cells with altered p53 showed increased MET-dependent motility and invasion.
  • Wild-type p53 suppresses MET via miR-34 transactivation and SP1 inhibition; these pathways are impaired in p53-null cells.
  • MET overexpression and invasion were highest in p53-null cells.

Conclusions:

  • MET is identified as a critical effector of p53 in controlling cell invasion.
  • MET inhibition presents a potential antimetastatic strategy for p53-mutated cancers.
  • Alterations in the p53/MET regulatory network influence cancer invasion extent.

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