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The study, led by Deborah Leckband, a professor of chemical and biomolecular engineering, found that cadherins, which bind to growth factor receptors, sense mechanical forces and respond by altering cellular communication and growth
.
The findings were published in PNAS
.
When growth factor receptors bind to cadherin molecules in normal tissue, they are unable to communicate with growth factor proteins—the substances they need to promote tissue growth
.
However, the study shows that the effect of tension on cadherin binding disrupts cadherin's interaction with growth factors, thereby turning on growth signals in the tissue
To demonstrate how tension affects tissue growth, the researchers set up an experiment to see how human cancer cells convert mechanical information into biochemical signals in vitro, Leckband said
.
The team used a homemade "cell stretcher" in which cancer cells grow in thin layers on the surface of a flexible medium
.
When the cells were stretched, the researchers observed changes that could increase tissue growth and tumorigenesis
"This study demonstrates that cadherin uses force to turn on biochemical growth signals," Leckband said
.
By demonstrating these forcing-induced disruptions, we may be able to find a way to alter the cadherin molecule to prevent certain types of tissue from growing, such as metastatic transformation and tumorigenesis
The team has already observed the cadherin growth factor receptor complex in human epithelial tissue and plans to expand on this concept by studying ex vivo human breast tissue
.
Brendan Sullivan, Taylor Light, Vinh Vu, Adrian Kapustka, Kalina Hristova, Deborah Leckband.
Mechanical disruption of E-cadherin complexes with epidermal growth factor receptor actuates growth factor–dependent signaling .
