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Study of placenta unexpectedly leads to cancer gene
Date:12/16/2008

t, researchers set out to find SENP2 target proteins that could be involved in arresting cell growth.

In the journey, they discovered that p53 or proteins that modify p53 activity were harmed by the SENP2 deficiency. The consequence was that p53 could no longer perform its vital job as a tumor suppressor. When p53 is functioning normally, it acts as a crucial guardian of the genome, or a checkpoint, by fixing genetic mistakes as they arise.

But when the p53 molecule is aberrantly regulated, either by an outside virus or an inherited genetic abnormality, the risk of cancer is higher because p53 cannot perform its job.

Researchers also found that SENP2 indirectly regulates p53 activity through another protein called Mdm2, which was already known to be involved in some cancers. In cells lacking SENP2, the Mdm2 becomes trapped in the nucleus, and is unable to halt p53, allowing it to accumulate within the cell. This disruption leads to distinct problems in cell cycle progression and normal gene replication.


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Contact: Leslie Orr
Leslie_Orr@urmc.rochester.edu
585-275-5774
University of Rochester Medical Center
Source:Eurekalert

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