Caltech researchers explore how cells reconcile mixed messages in decisions ab...( PASADENA Calif.The cells in our body...)

PASADENA, Calif.The cells in our body are constantly receiving mixed messages. For instance, an epithelial cell might be exposed to one signal telling it to divide and, simultaneously, another telling it to stop dividing. Understanding the process by which these competing environmental cues are reconciledas well as understanding the cues themselvesmight allow bioengineers to promote tissue growth when and where it's needed, and to discourage it when and where it's not.

The tug-of-war between these two sets of influences, and the effects they have on tissue growth, are explained and explored in a paper authored by scientists from the California Institute of Technology (Caltech) and published online in the early edition of the Proceedings of the National Academy of Sciences (PNAS). The findings in the paper may have implications for our understanding of how cancer develops, as well as for how best to grow tissues in a laboratory.

In normal epithelial tissues, mature cells that are in contact with one another tend not to divide, explains Anand Asthagiri, assistant professor of chemical engineering at Caltech, and the paper's principal investigator. This process, known as contact inhibition, is one of the ways the body keeps cell growth in check. When contact inhibition is disrupted, you get uncontrolled growth and the formation of tumors.

But what Asthagiri and colleagues have found is that contact inhibition is not a "master switch" that overrides all other environmental signals. The human body is, after all, a complex environment. And in that complex environment, contact inhibition doesn'tcan'twork by itself. It is instead part of what Asthagiri calls a "tunable system," one that takes into account, and is influenced by, other signals. Among those are growth signals such as epidermal growth factor (EGF).

When Asthagiri and his colleagues studied the interplay between contact inhibition and EGF in groups of epithelial
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