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A gene family that suppresses prostate cancer
Date:3/13/2014

re signs of precancerous lesions early in development, but no cancer by 15 months of age. When miR-34 and p53 genes were both silenced together, the researchers observed full prostate cancer in the mice.

The findings revealed that "miR-34 can be a tumor-suppressor gene, but it has to work together with p53," Nikitin said.

In mice that had both miR-34 and p53 silenced concurrently, cancerous lesions formed in a proximal part of the prostrate ducts, in a compartment known to contain prostate stem cells. The early lesions that developed when p53 was silenced alone occurred in a distal part of the ducts, away from the compartment where the stem cell pool is located. This suggested there was another mechanism involved when p53 and miR-34 were jointly silenced.

Also, the number of stem cells in mice with both p53 and miR-34 silenced increased substantially compared with control mice or mice with only miR-34 or p53 independently silenced.

"These results indicated that together miR-34 and p53 regulate the prostate stem cell compartments," said Nikitin.

This is significant, as cancer frequently develops when stem cells become unregulated and grow uncontrollably, he said.

Researchers further found that p53 and miR-34 affect stem cell growth by regulating MET expression. In absence of p53 and miR-34, MET is overexpressed, which leads to uncontrolled growth of prostate stem cells and high levels of cancer in these mice.

Future work will further examine the role of p53/miR-34/MET genes in stem cell growth and cancer. The findings have implications for many types of cancer.


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Contact: Joe Schwartz
Joe.Schwartz@cornell.edu
607-254-6235
Cornell University
Source:Eurekalert

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