Research Finds Prostate Cancer can be Inhibited Without Disturbing Body Processes
The mechanism behind how a facultative enzyme governs tumour growth in prostate cancer patients has been detailed by researchers.
The mechanism behind how a facultative enzyme governs tumour growth in prostate cancer patients has been detailed by researchers. This is a feat that could offer new ways to control cancer without disturbing normal body processes.
A kinase is a type of enzyme the body uses to regulate the functions of the proteins required for cell growth and maintenance, and researchers have discovered that one in particular plays a key role in developing prostate cancer.
"It's known as Mnk, and although it appears not to be essential for normal cell maintenance, it's important for cancer growth," said Luc Furic, a postdoctoral researcher working with Dr. Nahum Sonenberg at McGill University's Goodman Cancer Research Centre and Department of Biochemistry.
This is a very significant finding because the body's chemical processes are highly complex and interrelated, meaning that targeting one cause of cancer often involves affecting the body's normal functions.
An important part of cancer research is about trying to find processes that can be inhibited or stopped without causing damages to normal tissue.
The chemical process Mnk uses is known as phosphorylation, and this process activates or inactivates the body's proteins, controlling mechanisms that can cause disease.
In this case, Mnk works with a protein known as eIF4E to synthesize proteins in the cell.
Researchers at the Centre hospitalier de l'Universite de Montreal Research Centre (CRCHUM), Universite de Montreal and McGill University engineered mice that were able to block the phosphorylation process of this protein, and discovered that these mice became resistant to prostate cancer growth.
"The PTEN gene and its protein act as a tumour suppressor," explained Fred Saad, researcher at the CRCHUM and at Universit� de Montreal's Department of Surgery.
The research was published in the Proceedings of the National Academy of Sciences and received funding from the National Cancer Institute of Canada (Canada Cancer Society), the National Institutes of Health, Canada, the Knut and Alice Wallenberg foundation and the Fonds de la recherche en sante du Quebec.
Source: ANI