Temptations to exceed the speed limit are always plentiful, but only reckless drivers give in to such impulses. Likewise, numerous growth factors always abound in our bodies, but only cancerous cells are quickly "tempted" by these chemicals to divide again and again. Healthy cells, in contrast, divide only after being exposed to growth factors for eight continuous hours. What happens during these eight hours in a healthy cell that resists the call to divide? And even more important, what fails to work properly in the cancerous cell during these same hours? Why do cancerous cells give in so easily to the influence of growth factors, dividing so readily?
Answers to these questions have emerged from a study by a multidisciplinary team of Weizmann Institute researchers published recently in Molecular Cell. The scientists found that when a cell first receives a signal from a growth factor, ten groups of genes, about 8,000 in total, become activated. Of these, one group, consisting of about ten genes governed by the tumor suppressor p53, is the most crucial: These genes prevent the cell from dividing. Only if the growth factor continues to affect the cell for eight hours does p53 release its grip on the cell's DNA, allowing it to divide. Like a careful driver who puts the brakes on before proceeding, the activation of p53 at the time the cell receives a growth factor signal serves as a "brake," preventing instant division. In this manner, the healthy cell ensures that it will not divide as a result of accidental, mistaken or otherwise superfluous growth signals, but only if the signal is continuous and necessary. In cancerous cells, this mechanism malfunctions because in most of them, p53 is defective or missing altogether, so that even a fleeting growth signal can cause them to divide, leading to cancerous growth.
This interdisciplinary study has resulted from a collaboration between three research teams at the Weizmann Institute, headed by
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| Contact: Yivsam Azgad news@weizmann.ac.il 972-893-43856 Weizmann Institute of Science Source:Eurekalert |