A new molecular mechanism has been discovered by researchers that causes a reduction in rate of progression of cancer and other disorders associated with abnormal multiplication or growth. This study was published in the journal of Cell.
“Cells normally monitor the availability of nutrients and will slow down or accelerate their growth and division accordingly. A key monitor of nutrients is a protein called the Target of Rapamycin (TOR), but we do not know the details of how this protein feeds signals downstream to control growth says Dr. Stephen Michnick, senior author and a University of Montreal biochemistry professor. He adds that, “we were surprised to find that TOR hooks up to a circuit that controls the exit of cells from division which in turn modulates the RNA message that codes for a key cell cycle regulator called B-cyclin”.
“, Dr. Michnick explained. “We also found that TOR acts through a previously unforeseen intermediary, a protein that makes small chemical modifications to proteins normally stabilize B cyclin “, he added. “We have known that starvation and a drug that mimics starvation, rapamycin, affects B cyclin synthesis, but we didn’t know how. Our studies now point to one mechanism”, noted Dr. Messier.
Dr. Zenklusen emphasized that, “this is an important finding with implications for our understanding on how the normal organism interprets its environment to control growth and it was a surprise to find a mechanism that works through the RNA that codes for a regulatory protein. Dr. Michnick adds, “rapamycin is a promising therapy for some cancers and other devastating maladies such as the rare lung disease called lymphangioleiomyomatosis (LAM). It remains to be seen whether the pathway we have discovered might be an alternative target for the development of therapeutics against these diseases.”
Source: University of Montreal
Reference: Vincent Messier, Daniel Zenklusen, Stephen W. Michnick. A Nutrient-Responsive Pathway that Determines M Phase Timing through Control of B-Cyclin mRNA Stability. 2013. Cell. doi.org/10.1016/j.cell.2013.04.035.
Copyright 2012 Medimoon.com. All rights reserved. No part of this site can be reproduced without our written permission.None found.