Thus, it's possible to find a level of growth factor that will override the contact inhibition signal only for the peripheral cells, and then to find a second level that will allow division throughout the cluster. In other words, says Asthagiri, "You can tune the system; you can make the periphery grow more quickly relative to the rest of the area, or you can get the entire cluster to increase in size all at once."
"This is useful," he adds, "in thinking about how to engineer organs and tissues. I believe that this can become an important building block, a part of the tool set, that allows us to grow multicellular structuresand, ultimately, tissuesin specific, spatial ways."
And as for cancer? It's long been assumed that contact inhibition acts as a sort of switch that, when present, prevents tumor formation and, when absent, results in cell overgrowth and cancer. "Our findings support a more graded perspective of contact inhibition," the researchers write in the PNAS paper. Keeping in mind that cancer is often the result of an accumulation of genetic damage, they say, it seems likely that each "hit" to a cell's DNA might subtly lower the threshold at which EGF is capable of overriding contact inhibition to promote unbridled cell division and tumor growth.
"This tunability of the threshold amount of EGF," the researchers write, "would seem to be a fragility in cell cycle regulation that is exploited during cancer development."
|Contact: Lori Oliwenstein|
California Institute of Technology