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New MIT protein can block cancer division, growth
06-08-2011
by Kelsey Kaustinen  |  Email the author
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CAMBRIDGE, Mass.—In a recent study, researchers at the Massachusetts Institute of Technology (MIT) and Brigham and Women's Hospital focused on another pivotal way to fight cancer: HER3, a receptor and a protein that spreads the signals that cause cancer cells to continually and abnormally grow and replicate. By shutting off this protein, the researchers found that cell division in cancerous cells could be slowed or stopped completely.
 
Related receptors, such as EGFR and HER2, are well-known and already used in cancer treatment, and early-stage trials have started to look at antibodies that directly target HER3. The receptor is often involved in ovarian and pancreatic cancer, which MIT Professor Linda Griffith, who led the research team with Harvard Stem Cell Institute and Brigham and Women's cardiologist Richard Lee, says is one factor that has researchers so interested in the receptor.
 
The study originated in a regenerative-medicine project by co-first author Luis Alvarez, who received his Ph.D. from MIT. Alvarez developed a series of paired proteins in his search to promote bone re-growth, ones that researchers thought might have the ability promote interactions between HER3 and EGFR, both of which are growth receptors. When the researchers noticed that the proteins seemed to shut off cell growth and migration, they used the proteins on cancer cells, which caused the cells to stop growing and, in some cases, die.  
 
"It was not something we were expecting to see — you don't expect to shut off a receptor with something that normally activates it — but in retrospect it seemed obvious to try this approach for HER3," Griffith, the School of Engineering Professor of Innovative Teaching in MIT's Department of Biological Engineering and director of the Center for Gynepathology Research, said in a press release. "We pursued it only because we had people in the lab working with cancer cells, and we thought, 'Since it had these effects in stem cells, let's just try this in tumor cells, and see if something interesting happens.'"  
 
Cancer cell division and replication is rife with problems. Whereas normal cells will stop division if they detect DNA damage, or will undergo apoptosis, or cell death, cancer cells continue to divide and replicate, a condition known as hyperplasia. When these cells replicate, creating daughter cells with damaged or abnormal DNA, which will also grow and divide more often than normal, it is known as dysplasia. Additionally, cancer cells do not exhibit contact inhibition, as the CancerQuest website explains, which leads to the formation of tumors. Cancer cells reproduce without the normal external signals, which CancerQuest, an education program at Emory University, likens to "a car moving without having pressure applied to the gas pedal." The cells, aided by HER3, can reproduce without the usual need for external signaling.
 
The MIT protein works by disrupting HER3's connection with HER2, which cripples HER3 since it has to pair with another receptor, usually HER2, to send out growth signals to the rest of the cell. The protein is a fused pair of neuregulin molecules, and while single molecules usually stimulate the HER3 receptor, paired neuregulin molecules bind two adjacent HER3 receptors, which blocks them from binding with the HER2 receptors as needed.  
 
In six different kinds of cancer cells in which HER3 is overexpressed, the protein worked to shut off growth in each one, even in a type resistant to drugs targeting the EGFR receptor.  
 
The next step for the protein is to develop a version more suited to being tested in living animals, a task the MIT and Brigham and Women's team is already working on. Testing will be undertaken under the leadership of Steven Jay, co-first author of the paper and a joint MIT/Brigham and Women's postdoc. MIT postdoc Elma Kurtagic and graduate student Seymour de Picciotto are also first authors of the paper, which was published online May 26, 2011 in The Journal of Biological Chemistry.      
 

SOURCE: MIT press release
 
Code: E06081100

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