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Protein and microRNA block cellular transition vital to metastasis
Date:2/25/2011

nnected EMT activation to cancer progression and metastasis. Recent studies tie EMT to gain of stem cell traits in normal and transformed cells.

Cell status depends on p53, miR-200c levels

A series of experiments established that the p53 protein activates the miR-200c gene to produce the microRNA and that expression of the protein and miR-200c moved up and down together.

  • Knockout experiments in normal breast epithelial cells consistently showed that p53 expression stifled the EMT transition.

  • Cells with reduced p53 changed into mesenchymal-like cells.

  • When miR-200c was overexpressed in cells with low levels of p53, the cells took on epithelial characteristics, indicating that p53 uses the microRNA to block or reverse the transition to mesenchymal-type cells.

  • Mutated p53 failed to produce miR-200c, increasing stem cells in the cell culture.

  • Tissue array analysis of gene expression in 106 human breast tumor samples showed that low p53 expression correlated with higher expression of two genes associated with EMT. Increased p53 raised levels of miR-200c and the expression of a gene associated with epithelial status.

Mutations of p53 occur in more than half of cancers and loss of p53 activity correlates with poor prognosis in several cancer types. Restoring functions lost by p53 mutation by re-expressing miR-200c might be a good therapeutic strategy for treatment of p53-deficient tumors, Hung said.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert  

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