Finding could one day lead to new treatments for diseases such as cancer
MONDAY, March 24 (HealthDay News) -- New insights about an on-off switch that controls cell growth could one day help identify targets for drugs to treat cancer and other diseases that involve unnatural cell growth, researchers are reporting.
The researchers at the Duke Institute for Genome Sciences and Policy found that if the switch is "on," then a cell will divide, even if it's damaged or the signal to grow disappears.
The on-off switch is part of the pathway that controls cell division, the process that creates new cells. Before a cell divides, it goes through a checklist to make sure everything is in order. If the cell senses a problem early on, it can halt the process. But once the cell passes what's called the restriction point, it can no longer stop division. This on-off switch controls the restriction point and therefore plays an important role in cell growth, according to the study.
The on-off switch is part of the Rb-E2F signaling pathway. Rb (retinoblastoma) is an important tumor suppressor gene, and E2F is a transcription factor that governs the expression of all the genes important for cell growth, the researchers explained.
This pathway is found in all multi-cellular life forms, from humans to plants. The pathway is triggered when a cell receives an external chemical signal to grow.
"The wiring diagram is fundamentally the same. It's very likely that different organisms have evolved a very conserved design principle to regulate their growth," study lead author Guang Yao, a postdoctoral fellow in Duke's department of molecular genetics and microbiology, said in a prepared statement.
In their study, Yao and colleagues also found that the switch is bistable -- once it's turned on by an external signal, it can stay turned on, even if the signal vanishes.
The study results are published in the April issue of the journal Nature Cell Biology.
The Biology Project at the University of Arizona has more about cells.
-- Robert Preidt
SOURCE: Duke University, news release, March 23, 2008
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