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Finding the missing link: uOttawa researcher’s discovery for cancer treatment and more
OTTAWA, November 14, 2012 — Dr. Derrick Gibbings, professor in the Faculty of Medicine of the University of Ottawa, and his research team have discovered a link that will help to develop better drugs for treating cancer and other neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s. The findings are published in the advanced online version of Nature Cell Biology.
In the last ten to twenty years, autophagy has been recognized as an essential process that helps cells cope with many types of infection or disease. “Essentially,” explains Gibbings, “autophagy, which literally means ‘self-eating,’ is a process whereby the cell can sense and eliminate dangerous or toxic materials from itself. It is a fascinating process that we sometimes portray a bit like PacMan operating in all of the cells in our bodies.”
The researchers discovered that that when autophagy was inhibited, levels of microRNA, which regulates many processes in the body from learning to cell growth and cancer, decreased as well. They found that proteins essential for the activity of microRNA within the cell were being degraded by malfunctioning autophagy, which contributed to cancer growth and spread. Gibbings believes that what he has discovered is the missing link that connects defects in autophagy and microRNA in cancer.
“It’s a new link between two things we thought were independent phenomena in cancer cells,” Dr. Gibbings said. He believes that this information may help drug companies develop better drugs for treating cancer.
Dr. Gibbings is working with colleagues from the Swiss Federal Institute of Technology, the Institut Pasteur and Imperial College London.
While Dr. Gibbings and his team did not examine other diseases where autophagy is known to be problematic, he believes that their work “opens up a new aspect for researchers to look into diseases such as Alzheimer’s, Parkinson’s and Huntington’s, where we know autophagy is defective. Our work suggests that, as a consequence, the microRNA pathway will not be working, and this may very well be an important contributor to the pathology that brings people to the hospital with these diseases.”