University of Rochester scientists discovered a gene mutation that impairs the placenta and also is influential in cancer development, according to a study published on-line in the journal PLoS Biology on Tuesday.
The research is the first to link the key placental gene, SENP2, to the well-known p53 protein, which is defective in 50 percent of all cancers.
Until now, the SENP2 gene's role in early embryo development was not known. As a result of making the connection between SENP2 and the potent cancer stimuli, it will be possible to gain more insight into the complex genetic network involved in cancer, and to develop new therapies, said the authors.
They have been investigating how cellular signaling triggered by gene mutations affect embryo development in mice. The goal is to better understand the genetic causes and possible treatments for a number of diseases. What they discovered was an unexpected interaction between an old player, p53, and a new player, SENP2.
SENP2 is highly expressed in trophoblast cells, which are the stem cells required to form the placenta. The placenta surrounds, protects and nourishes the developing fetus. While investigating disruption of placental formation in a mouse model, they observed that embryos lacking SENP2 failed to properly make placental tissue.
The failure occurred because the cells that give rise to the placental tissues had undergone cell cycle arrest, and were trapped in a state of suspended growth. Next, researchers set out to find SENP2 target proteins that could be involved in arresting cell growth.
In the journey, they discovered that p53 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. |
About Us 
